LIBRARY OF CONGRESS. 

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UNITED STATES OF AMERICA. 



V 



A HANDBOOK 



OF 



PATHOLOGICAL ANATOMY 



AND 



HISTOLOGY 



WITH AN INTRODUCTORY SECTION ON 

POST-MOETEM EXAMHSTATIONS 

AND 

THE METHODS OF PRESERYH^G AISTD EXAMINING 

DISEASED TISSUES 



^ 



BY 



FRANCIS DELAFIELD, M.D., LL.D. 

PROFESSOR OF THE PRACTICE OP MEDICINE, COLLEGE OP PHYSICIANS AND SURGEONS, 

COLUMBIA COLLEGE, NEW YORK 



AND 

T. MITCHELL PRUDDEN, M.D. 

PROFESSOR OP PATHOLOGY AND DIRECTOR OP THE LABORATORIES OP HISTOLOGY, 

PATHOLOGY, AND BACTERIOLOGY, COLLEGE OP PHYSICIANS AND SURGEONS, 

COLUMBIA COLLEGE, NEW YORK 



FOURTH EDITION 

ILLUSTRATED BY 300 WOOD ENGRAVINGS PRINTED IN BLACK AND COLORS 






NEW YORK 



WILLIAM WOOD ct COMPANY^ 



I 



^^ 



Copyright by 
WILLIAM WOOD & COMPANY 

1892. 



PRESS OF 
STETTINER, LAMBERT A CO. 
£t, 14 4 26 READE STREET, 
NEW YORK. 



PREFACE 

TO THE F(3URTH EDITIOX 



In the fourth edition of this work the same objects have been 
kept in view as in former editions, but many parts have been largely 
rewritten and new drawings and microphotographs added. 

It is intended that the student and the practitioner shall find in it 
the information which they need to enable them to perform autopsies, 
to preserve the tissues, to prepare them properly, and to examine 
them with the microscope. 

The work, therefore, comprises instruction in the methods of 
making post-mortem examinations, of preserving diseased tissues, of 
preparing them for microscopical examination, and of examining 
and cultivating bacteria. It also gives an account of the lesions of 
the different parts of the body, of the infectious and general diseases, 
of violent deaths, and of poisoning ; of the changes produced by in- 
flammation and degeneration ; and of the structure of tumors. 

All of the drawings have been made by the authors. 

FRANCIS DELAFIELD, 
T. MITCHELL PRUDDEK 



CONTENTS. 



PART FIRST. 

THE METHOD OF MAKING POST-MORTEM EXAMINATIONS AND OF 
PRESERVING AND EXAMINING DISEASED TISSUES. 

The object in making post-mortem examinations. Causes of death, 3. — External 
Inspection, 4. — Cadaveric lividity, 4. — Putrefactive changes, 5. — Cooling of the 
body, 6. — Rigor mortis, 6. — Contusions, 7. — Wounds, fractures, scars, and tattoo 
marks, 8. — Internal Examination, 9. — The Head, 9. — Removal of calvarium, 
10. — The dura mater, 10. — The pia mater, 11. — The brain, 11. — Methods of open- 
ing the brain, 11-15. — Base of the cranium, 15. — Hardening and preserving the 
tissues for microscopical examination, 16. — The Spinal Cord, 17. — Preservation 
of cord and membranes, 18. —The Thorax and Abdomen, 18. — General inspection 
of abdominal cavity, 19. — The heart, 21. — The pleural cavities, 24.— The lungs, 
24. — Preservation of lungs and bronchi, 25. — Pharynx, larynx, and oesophagus, 
26. — Preservation of larynx and trachea, 26. — The Abdomen, 27. — Kidneys, 27. — 
Preservation of kidney, 28. — Suprarenal capsules, 29. — The spleen, 29. — Preserva- 
tion of suprarenal capsules and spleen, 29, 30. — Intestines, 30. — Preservation of 
intestines and stomach, 31, 32. — Stomach and duodenum, 31. — Liver, 32. — 
Preservation of liver, 33. — Pancreas, 33. — Genito-urinary Organs. Male organs, 
34. — Female organs, 35. — Bladder and uterus, 35. — Ovaries and Fallopian tubes, 
36. — Preservation of generative organs, 37. 

Autopsies in Cases op Suspected Poisoning, 37. 

Examination op the Bodies op New-born Children. General Inspection, 3§. — 
Internal Examination, 41. — Preservation of foetal and young tissues, 45. 

General Methods op Preserving Tissues and Preparing them for Study, 
46. — Fresh tissues, 46. — Decalcifying, 47. — Hardening and preservation, 47. — 
Miiller's fluid, alcohol, osmic acid, Flemming's osmic acid mixture, Delafield's 
osmic acid mixture, corrosive sublimate, chromic acid mixture, 47-50 — Embed- 
ding and section cutting, 50-52. — Staining, 52. — Preservation of museum speci- 
mens, 53. 

PART SECOND. 

CHANGES IN THE CIRCULATION OF THE BLOOD.— CHANGES IN 
THE COMPOSITION AND STRUCTURE OF THE BLOOD.— 
HYPERTROPHY, REGENERATION, DEGENERATION, 
ETC.— INFLAMMATION.— ANIMAL xiND VEGE- 
TABLE PARASITES.— INFECTIOUS DIS- 
EASES.— TUMORS. 

Changes in the Circulation op the Blood. Hypera^mia and An.-\?mia, 57. — 
Haemorrhage and transudation, 57. — Thrombosis and embolism, 59-62. 



VI CONTEXTS. 

Changes in the Composition and Structure of the Blood. Coagulability of 
the blood, 63. — Anaemia, 64. —Changes in the red blood cells, 64. — Changes in 
the white blood cells, 65. — Leukaemia, 66. — Melanaemia, 67. — Method of examina- 
tion of the blood, 67. — Foreign bodies in the blood, 69. 

Hypertrophy, Hyperplasia, Regeneration, jVIetaplasia. Hypertrophy and 
hyperplasia, 11.— Regeneration, 71. — Direct cell division, 72. — Indirect cell divi- 
sion, 72. — Metaplasia, 74. 

Degenerative Changes in the Tissues. Necrosis, 76. — Coagulation necrosis, 
76. — Cheesy degeneration, 77. — Parenchymatous degeneration, 77. — Fattj 
degeneration and fatty infiltration, 78. — Amyloid degeneration, 80. — Glycogen 
degeneration, 82. — Mucous degeneration, 82. — Colloid degeneration, 83. — Hyalin 
degeneration, 84. — Calcareous degeneration, 85.— Pigmentation, 85. 

Inflammation. Acute degeneration, 87. — Exudative inflammation, 88-94. — Exu- 
dative inflammation with production of new tissue, 94. — Healing of wounds, 94. 
—Healing of bone fractures, 98. — Croupous inflammation, 100. — Productive in- 
flammation, 101. — Special forms of inflammation, 102. 

Parasites. Animal Parasites. Protozoa, 103.— Worms, 106.— Arthropods, 116. — 
Methods of study and preparation of animal parasites, 117. 

Vegetable Parasites. Bacteria, 119. — Morphology and physiology of bacteria, 119. — 
The relations of bacteria to disease, 123.— Conditions influencing the occurrence 
of bacterial disease, 127. — Immunity and healing, 128. — Methods of studying bac- 
teria, 130. — Artificial cultivation of bacteria, 134. — Classification of bacteria, 
139. — Spheroidal bacteria, 140. — Rod-shaped bacteria, 142. — Spiral-shaped bac- 
teria, 144. — Yeasts, 145.— Moulds, 145.— Methods of studying yeasts and moulds, 
147. 

The Infectious Diseases. Infectious diseases induced by the pyogenic bac- 
teria, 149. — Erysipelas, 153. — Acute cerebro-spinal meningitis, 155. — 
Pyemia and septicemia, 157. — Infectious pseudo -membranous inflamma- 
tion of mucous membranes, 160. — Infectious diseases induced by the diplo- 
coccus pneumoniae:, 162. — Gonorrhcea, 165. — Anthrax, 167. — Tuberculosis, 
170. — Method of staining the tubercle bacilli, 177. — Lupus, 180. — Leprosy, 
182.— Syphilis, 184.— Rhinoscleroma, 186.— Glanders, 187.— Typhoid fe- 
ver, 189.— DiPHTHERL\, 198. — Tetanus, 201. — Influenza, 202. — Bacilli 
which are occasional inciters of infectious disease in man, 204. — Acti- 
nomycosis, 206. — Asiatic cholera, 209. — Relapsing fever, 213. — Small-pox, 
215. — Scarlet fever, 216. — Measles, 217. — Typhus fever, 218.— Hydro- 
phobia, 219. — Yellow fever, 220— The malarial fevers, 221. 

Tumors. Section I. General characters, 224. — Cause of tumors, 228.— Classi- 
fication of tumors, 231. — Cysts, 233. — Various lesions sometimes described as tu- 
mors, 235. — xNomenclature of complex tumors, 235. — Preservation of tumors, 
235. 

Section II. Special forms of tumors, 237. — Fibroma, 237. — Myxoma, 239. — 
Siarcoma, 241-249. —Endothelioma, 249. — Lipoma, 251. — Chondroma, 251. — 
Osteoma, 253. — Odontoma, 253. — Glioma, 254. — Myoma, 255. — Neuroma, 256. 
—Angioma, 258.— Epithelial tumors, 261.— Adenoma, 263.— Carcinoma, 265- 
276. 

PART THIRD. 

MORBID ANATOMY OF THE ORGANS. 

The Nervous System. The membranes of the brain, 229. — Hie dura mater f 
229.— Haemorrhages, 279.— Thrombosis, 280.— Inflammation, 280.— Tumors, 283. 



CONTENTS. Vii 

The pia mater, 284. — (Edema, 285.— Hypersemia and haemorrhage, 285. — In- 
flammatioQ, acute meningitis, 286. — Chronic meningitis, 290. — Tubercular 
meningitis, 291. — Syphilitic meningitis, 294. — Tumors, 294. — Parasites, 295. 
— The ventricles of the brain, 2^^. — Acute and chronic ependymitis, 296. — Con- 
genital hydrocephalus, 297. — Secondary hydrocephalus and primary hydroceph- 
alus in adults, 298. — Tumors, 298. — Pineal gland 2iXidi pituitary body, 299. 

The Brain, 300. — Thrombosis and embolism, 300-302. — Hyperaemia, anaemia, 
CBdema, and haemorrhage, 303, — Apoplectic foci, 304. —Secondary degenerations, 
306. — Hypertrophy and atrophy, 306. — Wounds, 307. — Holes or cysts in the 
brain, 308. — Inflammation of the brain, abscesses, 308. — Chronic interstitial en- 
cephalitis (sclerosis), 810. — Encephalitis in new-born, 311. — Syphilitic and tuber- 
cular encephalitis, 311, 312. — Lesions of brain in chronic paralysis of insane, 313. 
— Pigmentation, 318. — Tumors, 814. — Parasites, malformations, 315. 

Spinal Cord, 317. — Dura mater spinalis. Haemorrhages, inflammation, 317. — Tu- 
mors, 318. — Parasites, 318. — Pia mater spinalis. Haemorrhages, inflammations, 
318. — Tumors and parasites, 319. — The cord. Haemorrhage, injuries, 319. — 
Secondary degenerations, 820. — Descending gray degeneration, 320. — Ascending 
gray degeneration, 321. — Inflammation, acute myelitis, 323. — Poliomyelitis an- 
terior, 324. — Chronic myelitis, chronic interstitial myelitis, chronic transverse 
myelitis, 325. — Multiple sclerosis, 326. — Posterior spinal sclerosis, 827.— Solitary 
tubercles, gummata, cysts, and tumors, 328. — Syringomyelia, 329. — Malforma- 
tions, 330. 

The Peripheral Nerves. Changes after division, 381. — Acute and chronic neu- 
ritis, 332. — Multiple neuritis, syphilitic and tubercular neuritis, leprous neuritis, 
tumors, 333. 

Preparation of nerve tissue for microscopical study, 333. 

The Respiratory System:. Larynx and Trachea, 336. — Malformations, 336. — 
Acute catarrhal laryngitis and tracheitis, 836. — Chronic catarrhal, suppurative, 
croupous, syphilitic, and tubercular laryngitis, 387, 338.— (Edema glottidis, 
tumors, 889. 

The Pleura. Hydrothorax, haemorrhage, inflammation, 340, — Pleurisy with produc- 
tion of fibrin, pleurisy with production of fibrin and serum, 841. — Pleurisy with 
production of fibrin, serum, and pus (Empyema), 345.— Chronic pleurisy, tuber- 
cular pleurisy, 347. — Tumors, 348. 

The Bronchi. Acute catarrhal bronchitis, 349. — Chronic catarrhal bronchitis, acute 
croupous bronchitis, chronic croupous bronchitis, 351. — Bronchiectasia, 352. — 
Tumors, 353, 

The Lungs. Malformations, injuries, congestion, and cedema, 854. — Haemorrhage, 
355. — Emphysema, 356. — Atelectasis, gangrene, 358, — Inflammation, classifica- 
tion, acute lobar pneumonia, 859. — Broncho-pneumonia, 364. — Secondary and 
complicating pneumonia, 369, — Pneumonia of heart disease, 370. — Interstitial 
pneumonia, 372. — Tubercular pneumonia, 373. — Acute miliary tuberculosis, 374. 
— Subacute miliary tuberculosis, 877. — Chronic miliary tuberculosis, 377. — Acute 
pulmonary phthisis, 379. — Chronic phthisis, 383. — Syphilitic pneumonia, 3S6. — 
Tumors, 387.— Parasites, 389. 

The Mediastinum. Inflammation, 389. — Tumors, 890. 

The Vascular System. Pericardium. Injuries, dropsy, haemorrhage, pneumoua- 
tosis, 392.— Inflammation, 393, 394.— Tumors, 894. 

The Heart. Malformations, 395. — Abnormal size and positions of heart, wounds and 
ruptures, 897.— Atrophy, 898. — Hypertrophy, 399.— Dilatation, 400.— Degenera- 
tions, 401-403. — Fatty infiltration, atrophy of pericardial fat, 403.— Myomalacia, 
fragmentation of endocardium, 404. — Inflammation, 404. — Simple acute endo- 



Vlll CONTENTS. 

carditis, 405. — Mycotic endocarditis, 406, — Chronic endocarditis, 408. — Chronic 
ulcerative and tubercular endocarditis, 409. — Myocarditis, 409. — Changes in heart 
valves, aneurism of the heart, thrombosis of the heart, 410, 411. — Tumors and 
parasites, 412. 

The Blood Vessels. Atrophy and hypertrophy, 412. — Degeneration, 413. — The Arteries. 
Inflammation, acute arteritis, chronic arteritis, 414. — Tubercular arteritis, 419. 
— Dilatation and aneurism, 419. — Aneurism of the different arteries, 421. — Ste- 
nosis, 422. — Ruptures and wounds, 423. — Tumors, 424. — The Veins. Dilatation, 
425. — Wounds and rupture, inflammation, 426. — Tumors and parasites, 428. — 
• The Capillaries, 4l%^. — The Lymph Vessels, 428. — Inflammation, 429. — Lymphan- 
giectasis, tumors, 430. — The Lymph Nodes, 430. — Inflammation, acute inflam- 
mation, 431. — Chronic inflammation, 433. — Pigmentation, 434. — Inflammation 
with cheesy degeneration, 435. — Tubercular inflammation, 436. — Syphilitic in- 
flammation, 437. — Degenerations, 438. — Hyperplasia, 439. — Tumors and para- 
sites, 440. 

The Alimentary Canal, 293. — The Mouth. Malformations, 441. — Hypertrophy of 
cheeks and lips, inflammation, stomatitis, stomatitis ulcerosa, 442. — Syphilitic 
and tubercular stomatitis, gangrene, 443. — Tumors, 443. — The Tongue, Malfor- 
mations, hypertrophy, 444. — Inflammation, tumors, 445. — Ihe Pharynx and 
(Esophagus. Malformations, 446. — Inflammation, 447. — Ulceration, 448. — Dilata- 
tion of oesophagus, 449. — Stenosis, tumors, 450. 

The Stomach. Malformations, post-mortem changes, 453. — Injuries, hoemorrhage, 
inflammation, 454. — Ulcers, 457. — Dilatation, tumors, 460. — Degenerations, 463. 
— The Lntestines. Malformations, 463. — Incarceration, 464. — Intussusception, 
465. — Transposition, wounds and ruptures, 466 — The Small Intestine. Inflam- 
mation, 466. — Lesions of solitary and agminated nodules, 467. — Emboli, 468. — 
Large Intestine. Inflammations, 468. — Tumors, 475. — Concretions, parasites, 
477. 

The Peritoneum. Malformations, inflammations, 478. — Acute peritonitis, cellular 
peritonitis, exudative peritonitis, 479. — Chronic peritonitis, 482.^Chronic perito- 
nitis with adhesions, chronic peritonitis with thickening of peritoneum, and with 
production of serum, fibrin, and pus, 483, 484. — Hsemorrhagic peritonitis, tuber- 
cular peritonitis, 485. — Tumors, 486. — Parasites, 488. 

The Liver. Malformations, acquired changes in size and position, 489. — Anaemia 
and hypersemia, 490. — Wounds, rupture and haemorrhage, lesions of hepatic 
artery, lesions of portal vein, 492. — Lesions of hepatic veins, atrophy of liver, 
degenerations, 494. — Pigmentation, 498. — Acute yellow atrophy, 499. — Inflam- 
mation, acute hepatitis (abscess), 500. — Chronic interstitial hepatitis (cirrhosis), 
503,— Syphilitic hepatitis, 506. — Tubercular hepatitis, 507. — Perihepatitis, 508. — 
Hyperplasia of lymphatic tissue in the liver, tumors, 509. — Parasites, 512. 

The Biliary Passages and Gall Bladder. Catarrhal inflammation, 514. — Suppurative 
and croupous inflammation, 515. — Constriction, occlusion, and dilatation, 516. 
—Biliary calculi, 516.— Tumors, 518. 

The Spleen. Wounds, rupture and haemorrhage, 519. — Disturbances of the cir- 
culation, 520. — Infarctions, 521. — Inflammation, acute hyperplastic splenitis, 
522. — Suppurative and indurative splenitis, 523. — Syphilitic splenitis, tu- 
bercular splenitis, 525. — Perisplenitis, 526. — Alterations of spleen in leukaemia 
and pseudo-leukaemia, 526. — Degenerations, 527. — Pigmentation, tumors, 528. — 
Parasites, 528. — Malformations and displacements, 529. 

The Pancreas, Haemorrhage and inflammation, 530.— Degenerations, 531. — Tu- 
mors, malformations and displacements, 533. 

The Salivary Glands. Inflammation, 535.— Tumors and parasites, 536. 



CONTENTS. IX 

The Thyroid Gland. Hyperaemia, inflammation, degenerations, and tumors, 537. 
— Parasites, malformations, 539. — Myxoedema, 539. 

The Thymus Gland, 540. 

The Suprarenal Capsules. Malformations, hajmorrhage, thrombosis, inflamma- 
tion and degeneration, 541. — Tumors, 542. 

The Urinary Apparatus, 543. — The Kidneys. Malformations and changes in 
position, 543. — Bright's disease, classification, 544, —Congestion, acute de- 
generation, 544. — Acute exudative nephritis, 546.— Acute difFuse nephritis, 
549. — Chronic Bright's disease, 551. — Chronic congestion, chronic degene- 
ration, 551. — Chronic diffuse "nephritis with exudation, 552. — Chronic diffuse 
nephritis without exudation, 553. — Suppurative nepliritis and pyelo-nephritis, 555. 
♦ — Tubercular nephritis, 557. — Embolism and thrombosis, 557. — Hydronephrosis, 
558. — The cystic kidney, 559.— Perinephritis, 560. — Renal calculi, tumors, 561.— 
Parasites, 563. 

The Urinary Bladder. Malformations, 563. — Changes in size and position, 564. — 
Rupture and perforation, disturbances of circulation, 565. — Inflammation, acute 
catarrhal cystitis, chronic cystitis, 566. — Croupous and tubercular cystitis, 567. — 
Tumors, cysts, parasites, 568. — Calculi, 569. 

The Urethra. Congenital malformations, and changes in size and position, 570. — 
Strictures, wounds, ruptures and perforations, 571. — Inflammation, catarrhal 
urethritis, gonorrhoea, 572. — Croupous, syphilitic, and tubercular urethritis, tu- 
mors, 573. 

The Organs of Generation, 405. — Female. The Vulva. Malformations, hgemor- 
rhage, and hyperaemia, 574. — CEdema, inflammations, gangrene, 575. — Lupus, 
tumors and cysts, 576. 

The Vagina. Malformations, changes in size and position, 577. — Wounds, perfora- 
tions, inflammations, 578. — Tumors and parasites, bid.— The Uterus. Malforma- 
tions, 580. — Changes in size, 581. — Changes in position, 582. — Rupture, perfo- 
ration, hyperaemia, and haemorrhage, 584. — Inflammation, 585. — Puerperal 
inflammation, 587. — Ulceration, degeneration, tumors, 591. — Parasites and cysts, 
599. — The Ovaries. Malformations, changes in size and position, hyperaemia, 
haemorrhage, 600. — Inflammation, 601. — Tumors, 604. 

The Fallopian Tubes. Malformations, changes in position and size, 611. — Heemor- 
hage, inflammation, 612. — Tumors, extra-uterine pregnancy, 613. 

The Placenta. Haemorrhage, 614. — Inflammation, degenerations, 615, 

The Mamma. Malformations, haemorrhage, inflammation, 616. — Tumors, 619. 

Organs OF Generation. Male. The Penis. Malformations, 622. — Inflammation, 
tumors, 624. — The Scrotum, 625. — The Testicles. Malformations, hydrocele, 6.6. 
— Spermatocele, 627. — Haematocele, inflammation, 628. — Tumors, 631. — Para- 
sites, 632. — The Seminal Vesicles, 632. — The Prostate. Hypertrophy, 632.— In- 
flammation, tumors, 633. — Parasites, concretions, 634. — Cowpefs Glands, 634. — 
The Male Mamma, 634. 

The Bones. Disturbances of circulation, injuries, 635. — Inflammation, 636. — Peri- 
ostitis, 636. — Osteitis, 638. — Osteomyelitis, 644. — Necrosis, 646.— Caries, rach- 
itis, 647. — Osteomalacia, 650. — Alterations of the bone marrow in leukaemia and 
anaemia, 651. — Atrophy, tumors, 652, — Parasites, 655. 

Diseases of the Joints. Inflammation, 656. — Tumors, 659. 

Muscle. Haemorrhage, infarction, wounds and ruptures, inflammation, 661. — Atro- 
phy, 664. — Pseudo-hypertrophy, 667.— Degenerations, 667.— Hypertrophy. <6(S'^.. 
— Tumors, parasites, 669. 



X CONTEXTS. 

PART FOURTH. 

THE LESIONS FOUND IN THE GENERAL DISEASES, IN POISONING, 

AND IN VIOLENT DEATHS. 

Diseases Characterized by Alterations in the Composition of the Blood. 
Chlorosis, Pernicious Anemia, 673. — Addison's Disease, 674. — Leuke- 
mia, 675. — FsETJ'Do■LKTJK^^,llA (Hodgkiii's Disease), 675. 

Scorbutus, Purpura, 676. — Hematophilia, 677. 

Gout, 678. 

Diabetes, 679. 

Sunstroke, 680. 

Death from Burning, 681. 

Death from Electricity, 683. 

Death FROM Suffocation, Asphyxia, Q8d.— Death from StroAigulation^ Hanging, 
684. — Death from Drowning, 685. — External examination, 685. — Internal exam- 
ination, 686. 

Death from Poisoning, 688.— Sulpliuric acid, 688. — Nitric acid, 689. — Hydroclilo- 
ric, oxalic, and tartaric acids, 690. — Potasli and soda and their carbonates, am- 
monia, potassium nitrate, and phosphorus, 691. — Arsenic, 692. — Corrosive sub- 
limate, lead, 694. — Copper, tartar emetic, vegetable irritants, 695. — Cantharides, 
opium, poisonous fungi, and hydrocyanic acid, 696. — Carbolic acid and alcohol, 
697. — Chloroform, ether, chloral hydrate, strychnia, nux vomica, 698. — Conium, 
aconite, belladonna, lobelia, aigitalis, stramonium, carbonic oxide, and carbonic 
acid, 699. 



LIST OF ILLUSTEATIOIsTS. 



Fig. 
1. 

2. 

3. 

4. 
5. 

6. 

7. 
8. 

9. 

10. 
11. 
12. 
13. 
14. 
15. 
16. 
17. 
18. 
19. 
20. 
21. 
22. 
23. 

24. 
25. 
26. 
27. 
28. 
29. 
30. 
31. 
33. 
33. 
34. 
35. 



tubercle of 



Side view of the human brain, showing its fissures and convolutions, . 
View of the base of the brain, with the temporal lobes turned backward 

and outward, 

Drawing of the brain axis, separated from the brain mantle 

Phases of mitosis, or indirect cell division, 

Cheesy degeneration (coagulation necrosis) in miliary 

lung, 

Fatty degeneration of heart muscle, 

Fatty infiltration of liver cells, 

Amyloid (waxy) degeneration of capillaries of a glomerulus in the 

kidney, . . . ■ 

Corpora amylacea, 

Mucous degeneration of epithelial cells, 

Mucous degeneration of fibrous tissue of mamma, . 

Colloid degeneration of epithelial cells, . 

Hyalin degeneration of capillary blood vessels, 

Pigmentation of connective-tissue cells of the lungs, 

Emigration of white blood cells in infiamed bladder of frog, 

Pus cells from catarrhal inflammation of bronchial mucous membrane. 

Omentum of dog, showing peritonitis on fourth day. 

Developing blood vessels in new-formed tissue, 

Granulation tissue from wound of skin, 

Fibroblasts from granulation tissue, 

Cicatricial tissue, ... 

Exuberant granulations, 

New- formed cartilage and osteoid tissue from callus 

the femur, 
Croupous inflammation of trachea, 
Amoeba coli, 
Coccidium oviforme. 



Balantidium coli, 

Cercomonas intestinalis, 

Trichomonas vaginalis, 

Distoma hepaticum. 

Head of Taenia solium, 

Head and proglottides of Taenia mediocai 

Cuticula of echinococcus cyst, 

Scolices of Taenia echinococcus, 

Hooklets from scolex of Taenia echinococcus. 



ellata. 



fter 



fracture of 



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Xll 



LIST OF ILLUSTRATIONS. 



FIG. 

36. 
37. 
38. 
39. 
40. 
41. 
42. 
43. 
44. 
45. 
46. 
47. 
48. 

49. 

50. 
51. 
52. 
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54. 
55. 
56. 
57. 
58. 
59. 
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67. 
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70. 
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82. 



of the kidney 



Ascaris lumbricoides, 

Oxyuris vermicularis, 

Eggs of nematode worms, 

Trichocephalus dispar, 

Trichinae encysted in muscle, 

Filaria sanguinis hominis, 

Sarcoptes hominis, . 

Pediculus capitis, 

Drawing of three typical forms of bacteria illustrating the three classes, 

Bacteria with capsule, 

Bacilli showing spores. 

Bacilli showing cilia. 

Bacterial embolus in the blood vessels of the glomerulus 

in malignant ulcerative endocarditis, 
Colonies of micrococci in a blood vessel of the kidney, causing a small 

abscess, . . . 

A potato culture, 

A gelatin tube culture, ..... 
A gelatin plate culture of drinking water, 
Petri's plate culture of bacteria from the mouth. 
Spheroidal bacteria, . . . 

Sarcince, ........ 

Bacilli in pairs, 

Bacilli arranged end to end, forming chains, . 

Curved bacilli, forming spiral chains, 

Leptothrix buccalis with micrococcus colonies, 

Spirillum serpens, . 

Spirochgete denticola. 

Yeast, 

Aspergillus glaucus, 

Achorion Schonleinii, 

Staphylococcus pyogenes aureus, 

Staphylococcus pyogenes aureus, in and among the pus cells in an ab 

scess of the kidney, 
Streptococcus pyogenes. 
Erysipelas of the skin, 
Streptococci in masses in the blood and lymph vessel 

erysipelas, 
Micrococci in masses in the fibrinous exudation of pyaemic pleurisy 
Infectious croupous inflammation of the trachea. 
Streptococcus of croupous inflammation, 
Diplococcus pneumoniae, ..... 
Gonococci contained in pus cells, 

Micrococcus gonorrhoeae 

Anthrax of the skin, ..... 

Bacillus anthracis in blood vessels of the liver, 
Bacillus anthracis, ...... 

A nodule of tubercular inflammation (miliary tubercle) in the lung, 
A miliary tubercle from a lymph node, . 
Diffuse tubercle tissue from acute phthisis, 
A tubercle granulum from the pleura, . 



of the skin in 



PAGE 
111 
112 

112 
113 
114 
116 
117 
117 
120 
120 
121 
122 

124 

125 

135 
136 
137 
138 
141 
141 
142 
142 
142 
143 
144 
144 
145 
145 
146 
149 

150 
152 
153 

154 
158 
160 
161 
162 
165 
166 
167 
168 
169 
170 
171 
172 
17a 



LIST OF ILLUSTRATIONS. 



[Ill 



FIG. 

83. 
84. 

85. 

86. 

87. 

88. 

89. 

90. 

91. 

93. 

93. 

94. 

95. 

96. 

97. 

98. 

99. 
100. 
101. 
102. 
103. 
104. 
105. 
106. 
107. 
108. 
109. 
110. 
111. 
112. 
113. 
114. 
115. 
116. 
117. 
118. 
119. 
120. 
121. 
122. 
123. 
124. 
125. 
126. 
127. 
128. 
129. 
130. 
131. 
132. 



Tubercle bacilli, with pus cells, in sputum, . 
Inflammatory nodule in the liver of the rabb 

bercle bacilli, 

Lupus of face, 

The bacilli of leprosy 

Small nodule of syphilitic inflammation (miliary g 
New-formed tissue in syphilitic inflammation, 

Bacillus mallei, 

Cluster of typhoid bacilli in the spleen, . 

Bacillus typhosus, 

Bacillus diphtheriae, 

Diphtheritic inflammation of the tonsil, . . . 

Bacillus tetani, 

Actinomyces bovis, 

Actinomyces growing in human bronchus, 
Spirillum cholerae Asiaticae, .... 

Spirochaete Obermeieri, 

A small-pox vesicle of the skin, 
The hsematozoon of malaria, . . 
Epithelial cell "inclusions" in tumors, . 
Dense fibroma of abdominal wall, . 
Small papilloma of the skin, . . 
Myxoma of subcutaneous tissue of back, 
Myxoma growing into abdominal cavit}', 
Mucous polyp of the nose, .... 
Large spindle-celled sarcoma of humerus. 
Small spindle-celled sarcoma of forearm, 
Small round-celled sarcoma of liver, 
Large round-celled sarcoma of leg, 
Melano-sarcoma from submaxillary region, 
Giant-celled sarcoma of bonr^, .... 
Angio-sarcoma of liver, . . . 
Myxo-sarcoma of pharynx, ... 
Adeno-sarcoma of parotid, .... 
Endothelioma of dura mater, .... 
Chondroma of subcutaneous connective tissue, 
Myxo-chondroma of cervical region, 

Glioma of brain, 

Neuroglia or " spider" cells from glioma of brain, 

Myoma of uterus, 

Neuroma ganglioniforme, ' . . . . 
Fibroma (false neuroma) of lumbar nerve. 
Multiple fibromata of pneumogastric nerve, . 
Angioma telangiectoides, .... 

Angioma cavernosum of liver, 
Congenital lymphangioma from arm of child. 

Adenoma of mamma 

Adenoma of stomach 

Adenoma of antrum, ..... 
Cancer cells infiltrating the tissue near a tumor. 
Metastatic carcinoma in l3"mph vessels of the ploui 







PAGE 


. . 


175 


produced by dead tu 




t i. 


176 


• . , 


180 


• . • . 


183 


•umma) in the liver. . 


184 


• • < • 


185 


• • • . 


188 


• • • 


195 


• • fi « 


196 


• « • e 


198 


o F a 


199 


O f. * » 


201 


• CO* 


206 


• » • o 


207 


« •> e o 


210 


• o «. « 


213 


• o • • 


215 


• e • • . 


222 


9 


230 


o o « e 


237 


oca* 


238 


o . « 


239 


• ceo 


240 


o « • o 


241 


« o e o 


243 


• » • • 


243 


• * o • 


244 


o o « . 


244 


« o o * 


245 


* o o o 


246 


O > B O 


247 


OS.. 


248 


• • • 




249 


• 




. " 350 


• o a 




253 


• O 




252 


• e • 




254 


r • 




254 


• • • 




355 


• • 




257 


. 




258 


• « • 




258 


• . • 




259 


• . • 




360 


. 




360 


• • • ■ 




363 


• . « 




364 


• 




364 


<• • S . 


367 


1-a, 


. 


368 



^ 



XIV 



LIST OF ILLUSTRATIONS. 



the pia mater 



em- 



FIG. 

133. Inflammation in carcinoma uteri, .... 

134. Epithelioma of the neck, 

135. Epithelioma of axillary Ijoiph node, . . . 

136. Epithelioma of back of hand, .... 

137. A small epithelioma of the side of the nose, . 

138. Epithelioma of nose, 

139. Carcinoma mammse, scirrhus, .... 

140. Medullary carcinoma of the stomach, 

141. Colloifl carcinoma of rectum, .... 

142. Carcinoma myxomatodes mammse, 

143. Chronic pachymeningitis interna hgemorrhagica, . 

144. Brain sand, 

145. Acute cellular meningitis 

146. Acute exudative meningitis, . 

147. Fatty degeneration of cells along the blood vessels of 

after exudative meningitis, .... 

148. A miliary tubercle of the pia mater, 

149. A miliary tubercle of the pia mater — cheesy degeneration, 

150. A miliary tubercle of the pia mater, 

151. Miliary tubercles of the ependy ma, 
153. A miliary tubercle of the ependyma, 

153. Congenital hydrocephalus in child, 

154. Degenerated cells, cholesterin crystals, etc., from brain tissue in 

bolic softening of brain, 

155. Blood vessels from an area of embolic softening of brain, 

156. Syphilitic obliterating endarteritis of a cerebral artery, 

157. Solitary tubercle of cerebellum, .... 

158. Descending gray degeneration, .... 

159. Ascending gray degeneration, 

160. Ascending gray degeneration, .... 

161. Degenerated tissue from acute myelitis, 

162. Poliomyelitis anterior, 

163. Poliomyelitis anterior, 

164. Posterior spinal sclerosis, 

165. Posterior spinal sclerosis, 

166. Syringomyelia, . . . . 

167. Hydromyelia, 

168. Multiple neuritis, 

169. An ulcer of the larynx in chronic catarrhal laryngitis, 

170. Tubercular laryngitis, 

171. Artificial pleurisy in dog, twenty-four hours' duration, 

172. Artificial pleurisy in dog on fifth day, 

173. Tubercular pleurisy, 

174. Acute catarrhal bronchitis, . . . . 

175. Section of the wall of a bronchiectasia, . 

176. Emphysema, showing holes in the walls of the air vesicles, . 

177. Acute lobar pneumonia ; pneumococci in the exudation, 

178. Acute lobar pneumonia with organized tissue in the air spaces, 

179. Pneumonia showing organized tissue in an air vesicle, . 

180. Lobar pneumonia with organized tissue in air vesicles ; blood vessels 

injected, 



PAGE 

268 
270 
271 
271 
272 
272 
273 
274 
275 
275 
282 
282 
287 
288 

289 
290 
291 
291 
292 
293 
297 

301 
302 
311 
312 
321 
322 
332 
323 
324 
325 
336 
327 
329 
331 
332 
337 
338 
343 
344 
348 
350 
353 
357 
360 
361 
363 

363 



LIST OF ILLUSTRATIONS. 



XV 



FIG. 

181. Broncho-pneumonia in a child, 

182. Bronchopneumonia in an adult, 

183. Persistent broncho-pneumonia, 

184. Persistent broncho-pneumonia, 

185. Lobular pneumonia in a child, complicating diphtheria, showing strep- 

tococci, 

186. The pneumonia of heart disease, 

187. Interstitial pneumonia 

188. A miliary tubercle in the luEig, 

189. A miliary tubercle, 

190. A miliary tubercle, 

191. A peribronchitic miliary tubercle, . 

192. Miliary tubercle in lung of child, showing tubercle bacilli, 

193. An aggregation of miliary tubercles, 

194. Diffuse tubercular inflammation, 

195. An area of coagulation necrosis surrounded by a zone of pneumonia 

196. Tubercular inflammation about bronchus, 

197. Acute phthisis with dilatation of bronchi, 

198. Chronic phthisis, 

199. Chronic phthisis, 

200. Chronic phthisis, 

201. Chronic phthisis — intra-alveolar pneumonia, 

202. Interstitial pneumonia of chronic phthisis, 

203. An old miliary tubercle, .... 

204. Tubercle tissue around an area of coagulation necrosis, 

205. Interstitial syphilitic pneumonia, 

206. Primary carcinoma of the lung, 

207. Fatty degeneration of the heart muscle, . 

208. Fatty infiltration of the heart, 

209. Atrophic pericardial fat, . 

210. Vegetation on aortic valve, . . . 

211. Mycotic endocarditis, .... 

212. Chronic endocarditis, .... 

213. Chronic endocarditis, .... 

214. Chronic interstitial myocarditi.<, 

215. Chronic arteritis, 

216. Chronic obliterating endarteritis 

217. Chronic arteritis, 

218. Chronic inflammation of the aorta, 

219. Atheroma of the aorta 

220. Tubercular arteritis in the lung, 

221. Tubercular phlebitis, .... 

222. Acute inflammation of lymph node in typhoid fever, 

223. Chronic inflammation of bronchial lymph node, 

224. Pigmentation of bronchial lymph node, . 

225. Section of the wall of a cyst of the neck, 

226. Section of the wall of a cyst of the neck, 

227. Adenoid polyp of pharynx, 

228. Diffuse sarcoma of the pharynx, 

229. Catarrhal colitis, 

230. Catarrhal colitis, productive and necrotic, 



PAGE 

365 
366 
367 

368 

369 
370 
371 
372 
373 
374 
375 
376 
377 
378 
379 
380 
380 
381 
382 
382 
383 
384 
385 
386 
387 
388 
401 
402 
403 
405 
406 
407 
408 
410 
415 
416 
417 
418 
418 
419 
427 
432 
oo 
434 
446 
447 
451 
452 
469 
469 



XVI 



LIST OF ILLUSTRATIONS. 



FIG, 

23L Catarrhal colitis, productive and necrotic, 

232. Croupous colitis, 

233. Follicular (nodular) colitis, 

234. Acute cellular peritonitis, 

235. Acute exudative peritonitis, 

236. Chronic cellular peritonitis, 

237. Chronic peritonitis vt^ith adhesions, 

238. Section of a retroperitoneal sarcoma, . • . 

239. Chronic congestion of the liver, 

240. Fatty infiltration of liver cells, 
241 Fatty infiltration of liver, 

242. Amyloid degeneration of the liver, 

243. Pigmentation of the liver in malarial fever, . 

244. Chronic interstitial hepatitis 

245. Chronic interstitial hepatitis, .... 

246. Syphilitic hepatitis, 

247. Gumma of liver, . . . 

248. Echinococcus multilocularis of the liver, 

249. Primary carcinoma of the common bile duct, 

250. Congestion of the spleen, .... 

251. Chronic indurative splenitis, .... 

252. Chronic interstitial splenitis, . , . . 

253. Malarial spleen, 

254. Amyloid degeneration of glomeruli of the spleen, 

255. Fat necrosis in the pancreas, .... 

256. Colloid struma, 

257. Section of the atrophied thyroid gland in myxoedema, 

258. Acute degeneration of the kidney, .... 

259. Acute nephritis, ....... 

260. Acute nephritis occurring with acute general tuberculosis, 

261. Acute nephritis, 

262. Acute diffuse nephritis. . . . : . 

263. Chronic diffuse nephritis, .... 

264. Chronic nephritis without exudation, 

265. Waxy degeneration of tuft capillaries, . 

266. Cysts of the kidney, o . » . . 

267. Vaginal epithelium, ...... 

268. Chronic endometritis with polypoid outgrowth, 

269. Adenomatous hyperplasia of the uterine mucous membrane, 

270. Chronic endometritis, 

271. Uterine phlebitis, .... 

272. Adenoma of the uterus, . 

273. Adenoma of the uterus, . 

274. Carcinoma of the cervix uteri, 

275. Carcinoma (epithelioma) of the uterus, 

276. Chronic oophoritis, .... 

277. Chronic oophoritis, .... 

278. Commencement of sarcomatous growth in fh^e ovary, 

279. Papilloma of peritoneum, 

280. Cystic adenoma of ovary, 

281. Cells from contents of an ovarian cyst. 



PAGE 

470 

472 

473 

480 

481 

482 

484 

487 

491 

496 

496 

497 

498 

502 

504 

506 

507 

514 

517 

520 

524 

524 

525 

528 

532 

538 

539 

545 

546 

547 

548 

550 

553 

554 

555 

559 

579 

586 

587 

588 

590 

595 

596 

597 

598 

602 

003 

604 

605 

606 

607 



LIST OF ILLUSTRATIONS. 



XVll 



FIG. 

282. Cystic adenoma of ovary, 

283. Multiple papillary cysts of the omentum 

284. Adeno- sarcoma of the ovary, . 

285. Hydro- salpinx, .... 

286. Suppurative mastitis, ... 

287. Chronic inflammation of mammary gland, 

288. Intracanalicular fibroma of the mamma, 

289. Pericanalicular fibroma, . 

290. Chronic interstitial orchitis, • . 

291. Chronic orchitis, 

292. Rarefying osteitis, . 

293. Condensing osteitis, 

294. Tubercular osteitis, 

295. Rachitic bone, ... 

296. Chronic interstitial myositis, . 

297. Progressive muscular atrophy, 

298. Progressive muscular atrophy, 

299. Pseudo-hypertrophy of gastrocnemius muscle, 

300. Hyalin degeneration of muscle, 



PAGE 

607 
608 
609 
611 
617 
618 
619 
620 
629 
630 
639 
641 
642 
648 
663 
664 
665 
666 
668 



PART I. 



THE METHOD OF MAKIjSTG 



•POST-MORTEM EXAMINATIONS 



AND OF 



PRESERVING 



AND 



EXAMIISriJfG PATHOLOGICAL TISSUES. 



THE METHOD 



OF MAKIKG 



POST-MORTEM EXAMINATIONS. 



The object in making a post-mortem examination varies in dif- 
ferent cases. It may be to determine whether a person has died 
from violence or poisoning ; to account for a sudden death ; or to 
study the lesions of disease. In any case the examination should 
embrace all the important parts of the body, not merely a suspected 
organ, and it should be recorded at the time it is made. 

In endeavoring to ascertain the cause of death, when the clinical 
history is imperfect or unknown, great care is necessary. Mechani- 
cal causes of death, which destroy life by abolishing the function of 
one of the important viscera, are relatively infrequent. Most of the 
lesions which we find after death indicate rather the ravages of dis- 
ease than the cause of death. We do not know how great a degree 
of meningitis, or of pneumonia, or of endocarditis, or of cirrhosis, or 
of nephritis necessarily causes death. On the contrary, we find that 
one patient recovers with an extent of lesion which is sufficient to 
destroy the life of another. So with accidents ; there is often no 
evident reason why fractures of the skull or of the pelvis should 
destroy life, but yet they usually do. In some of the general dis • 
eases, such as typhoid fever, the visible lesions cannot always be 
called the cause of death ; in others, such as typhus fever, there may 
be no evident lesions at all. Sudden deaths of persons who have 
apparently been in good health up to the time of death are often par- 



4 THE METHOD OF MAKING 

ticularly obscure. In many of them we have to acknowledge that 
we can find no sufficient cause for the death. This is of course due 
to our imperfect knowledge, but it is much better in such cases to 
avow our ignorance than to attribute the death to some trifling 
lesion. The brain and the heart are the organs which are especially 
capable of giving symptoms during life "s^-ithout corresponding 
lesions after death. Very well-marked cardiac or cerebral symp- 
toms may continue for days or months, and apparently destroy life, 
and yet after death we find no corresponding anatomical changes. 
It is the no^'ice in post-mortem examinations who is particularly apt 
to mistake ordinary post-mortem appearances for lesions. 

EXTERNAL INSPECTION. 

Before commencing the examination of the internal viscera it is 
always necessary to make some inspection of the external surface of 
the body. The minuteness of this inspection ^dll depend upon the 
character of the case. In the case of an unknown person, or of one 
suspected to have died from unnatural causes, it is necessary to 
search for and record not only all contusions, wounds, etc. , their 
size, situation, and condition, but also deforixiities from disease and 
any physical peculiarities of hair, eyes, teeth, moles, etc. , by which 
the person may be identified. In such cases it is well, if possible, to 
have a photograph taken of the entire body. In cases of doubtful 
identity it is sometimes wise to make a wax or plaster cast of the 
outside of the teeth and jaws. In ordinary examinations we note 
the general nutritive condition of the body, and look for evidences of 
external injury, for skin diseases, ulcers, oedema, gouty deposits, 
abscesses, enlarged lymphatic glands, etc. The glans penis and pre- 
puce are to be carefully searched for syphilitic cicatrices. 

It is usual to find certain changes in the external appearances of 
the body which are due to the cessation of hfe and the commence- 
ment of decomposition. We speak now of bodies which have not 
been buried, but which have been kept in the ordinary way, lyhig on 
the back, and looselv covered with a shroud or dressed ^^'ith the or- 
dinary clothes. 

Cadaveric Lividity. — After life becomes extinct, and before the 
blood coagulates, it settles in the veins of the more dependent parts 
of the body, producing, usually within a few hoiu's after death, a 
mottling of the surface with irregTilar li^'id patches. These patches 
may coalesce, forming a uniform dusky -red color over the back of 
the trunk, head, and extremities, and sometimes over the ears, face, 
and neck. The same effect is observed on the anterior aspect of the 
body if it has lain on the face. At points of pressure, from folds in 
the clothes or from the weight of the body on the table, the red color 



POST-MORTEM EXAMINATIONS. 

is absent or less marked. These changes occur before putrefaction 
sets in. This cadaveric Hvidity or hypostasis should not be mistaken 
for ante-mortem ecchymosis, from which it may usually be readily 
distinguished by its position and extent, by the fact that the surface 
of the skin is not elevated, and by the fact that on incision no blood 
is found free in the interstices of the tissues. ISTot infrequently the 
subcutaneous tissue in the vicinity of these post-mortem hypostases 
becomes infiltrated with reddish serum. Very soon after death, par- 
ticularly in warm weather, the tissues immediately around the sub- 
cutaneous veins of the neck and thorax and in other situations may 
become stained of a bluish-red color from the decomposition and 
escape from the vessels of the coloring matter of the blood. If the 
epidermis has been detached at any point, the skin beneath soon be- 
comes dry and brown. 

Putrefactive Changes. — Usually in from one to three days, de- 
pending upon circumstances, a greenish discoloration of the skin 
appears, at first upon the middle of the abdomen, over which it 
gradually spreads, assuming a deeper hue and often changing to a 
greenish purple or brown. Greenish patches may now appear on 
different parts of the body, earliest upon those overlying the internal 
cavities ; this discoloration is probably produced by the action on the 
haemoglobin of gases developed by decomposition. The eyeballs now 
become flaccid, and if the eyelids are not closed the conjunctiva and 
cornea become brown and dry. The pressure of gases developed by 
decomposition in the internal cavities not infrequently forces a 
greater or less quantity of frothy, reddish fluid or mucus from the 
mouth and nostrils, producing distention of the abdomen, and, if ex- 
cessive, may produce changes of position of the blood in the vessels, 
and even a moderate amount of displacement of the internal organs. 

After five or six days, under ordinary circumstances, the entire 
surface is discolored green or brown. After this the epidermis be- 
comes loosened from the formation of gases and separation of fluids 
beneath, and the tissues become flaccid. The abdomen and thorax 
may be greatly distended, the features distorted and scarcely recog- 
nizable from swelling, and the hair and nails loosened. Beyond this 
stage of putrefaction the consecutive changes, leading to more or less 
disintegration of the soft tissues, can scarcely be followed with cer- 
tainty. The rapidity with which these changes follow one another 
depends upon a variety of conditions, such as temperature, moist- 
ure, access of air, and the diseases which have preceded or caused 
death. Thus an elevated temperature and the presence of air and 
moisture hasten the advent and progress of putrefactive changes. 
The bodies of infants usually decompose more rapidly than those of 
adults, fat bodies more quickly than lean ones. The infectious dis- 



I 



6 THE METHUD OF MAKING 

eases, intemperance, and the puerperal condition promote rapid de- 
composition, as does also death from suffocating gases. Poisoning by 
arsenic, alcohol, antimony, sulphuric acid, strychnin, and chloro- 
form may retard the progress of decomposition. Burial in dry soil 
and submersion in water also retard the progress of decay. 

Cooling of the Body. — The internal temperature of the healthy 
liAuns; bodv is about 37.5^ C. (99.5' Fahr. ). But it mav be increased 
several des-rees in consequence of disease. After death the chemical 
changes upon which the maintenance of this temperature depends 
rapidly diminish, and the body gradually cools to the temperature of 
the surroimdins: meditun. This usuallv occurs in from about fifteen 
to twenty hours, but the time required depends upon a variety of con- 
ditions. Immediately after death there is, in nearly all cases, a 
shglit elevation of internal temperatiu'e, owing to the fact that the 
metabolic changes in the tissues still continue for a time, while the 
blood ceases to be cooled by passing through the lungs and periphe- 
ral capillaries. After death from certain diseases — yellow fever, 
cholera, rheumatic fever, and tetanus — a considerable elevation of in- 
ternal temperature has been repeatedly observed. The time occupied 
by the cooling of the body may be prolonged after sudden death 
from accidents, acute diseases, apoplexy, and asphyxia. A number 
of cases are recorded in which the bodv retained its heat for several 
days Tvithout kno^^m cause. 

After death from wasting chronic disease, and in some cases after 
severe haemorrhages, the cooling of the body is very rapid, the exter- 
nal temperature being reduced to that of the surrounding air within 
four or five hours. Fat bodies cool less quickly than lean ones, the 
bodies of well-nourished adults less quickly than those of children or 
old persons. The temperature of the surrounding medium, the de- 
gree of protection of the body from currents of air, will, of course, 
modify the progress of cooling : and the internal organs naturally 
retain their heat longer than the surface of the body. The rate at 
which cooling occurs is most rapid, as a rule, during the hours imme- 
diately following death, not^vithstanding the post-mortem rise which 
may ensue. 

It will thus be seen that if required to ^^ronounce upon the time 
which has elapsed since death in a given case, we can do so only ap- 
proximately. It is necessary to take into account all of the above- 
mentioned conditions which modifv the rate of coohnor of the bodv. 
and then we may be able to state only the probabilities of the case. 
It is furthermore unsafe in any case to infer the cause of death from 
the rate of cooling of the body. 

Bicjor Mortis. — Death is usually succeeded immediately by a pe- 
riod of complete muscular relaxation. The jaw drops and the limbs 



POST-MORTEM EXAMINATIONS. 7 

become flaccid. The muscles miay retain for two or three hours, 
however, the capacity of contracting on the appHcation of appropri- 
ate stimuli. On the average within six hours the muscles become 
firm and rigid. This post-mortem rigidity is called rigor mortis. 
On the occurrence of the rigor mortis the muscles become fixed in 
whatever position they may have had at the time of its occurrence. 
It usually begins in the muscles of the eyelids, extends to those of 
the back of the neck and lower jaw, then to the face and neck, and 
thence passing downward affects the muscles of the thorax and 
lower extremities. It usually disappears in the same order. Although 
commencing on the average six hours after death, it maj^ set in al- 
most instantly, or it may be delayed for twenty -four hours or more. 
It may pass off very rapidly, in rare cases in from one to three hours ; 
or it may persist for two or three weeks or longer. It may be said 
in general that the average time of its disappearance is within twen- 
ty-four or forty-eight hours after its occurrence, depending on tempe- 
rature, its intensity, the mode of death, the period of its advent, etc. 
Caspar states that in foetuses before term he has never observed rigid- 
ity, and that in young children it is feeble and of short duration. 
Its occurrence and phenomena may be in some cases of the highest 
medico-legal importance; but its careful observation does not, with 
our present knowledge of its significance, appear to essentially fur- 
ther the aims of the practical pathologist. ' 

Cofitusions. — It is often important to determine whether violence 
has been inflicted upon a body before death. In regard to this point, 
we must remember, first, that blows and falls of sufficient violence 
to fracture bones and rupture the viscera may leave no marks on the 
skin, even though the person has survived for several days ; and, 
second, that there are post-mortem appearances which simulate ante- 
mortem bruises. A severe contusion during life may present, at 
first, no mark or only a general redness. After a short time the 
injured part becomes swollen and of a red color ; this color may be 
succeeded by a dark blue, and this in turn fade into a greenish 
yellow or yellow ; these later appearances are due to an escape of 
blood from the vessels and to a subsequent decomposition of luiemo- 
globin. If therefore we cut into such an ecchymosis after death, we 
find extravasated blood or the coloring matter of the blood, in the 
form of pigment granules, free in the tissues. Post-mortem discolo- 
rations, on the other hand, although their external appearance may 
resemble that of ante-mortem ecchymosis, are not formed by an 
extravasation of blood, but by a circumscribed congestion of the 

' For further details concerning rigor mortis, putrefactive changes, particularly the 
later stages, and the phenomena of cooling of the body, see Tidy, " Legal Medicine," 
vol. i., pp. 52-120, or other works on medical jurisprudence. 



/' 



8 THE METHOD OF MAKIXG 

vessels or by an escape c»f blood-stained serrnn. If we cut into such 
discolorations. therefore,, we find no blood outside the vessels. 

Blows on the skin of a body which has not been dead for more 
than about two hours may produce true ecchynioses with extravasa- 
tion of blood, such as can be distinsruished with s-reat difficultv or not 
at all from those formed during life. If putrefactive changes be 
present the difficulty of distinguishing between ante-mortem and post- 
mortem bruises is greatly enhanced. 

Hanging and strangulation are attended with the formation of 
marks on the neck ^which are fully described in works on forensic 
medicine. These marks must not be confounded with the natural 
creases of the skin of the neck. Many adults during hfe have 
creases of the skin of the neck, one c-r more in number, runninsc 
downward from the ear under the chin or encu'chng the neck. After 
death these creases mav be much more evident than durins: life, and 
may be rendered more decided by the position of the head and the 
freezing of the body. They usually persist until the skin putrefies. 

TTounds. — AVe should notice the situation, extent, and direction 
of a wound . the condition of its edges and the surrounding tissues. 
If it be a deep, penetrating wound its course and extent should be 
ascertained by careful dissection rather than by use of a probe. 

If the edges of a wound be inflamed and suppurating, or com- 
mencing to cicatrize, it must have been inflicted some time l:>ef ore 
death. In a woim.d inflicted a short time before death the edsres are 
usually everted : there may be more or less extravasation of blood 
into the surrounding tissues, and the vessels contain coagula : but 
sometimes none of these changes are observed. The chief character- 
istics of a wound inflicted after death are. absence of a considerable 
amount of bleeding, non-retraction of the edges, and the absence of 
extravasation of blood into the tissues. But a wound inflicted within 
two hours after death mav resemble verv closelv one inflicted during: 
life. In general, unless a wound is old enough for its edges to pre- 
sent inflammatory changes, we must be very careful in asserting its 
ante-mortem or post-mortem character. 

Fractures. — It may be important to determine whether a bone 
was fractured before or after death. This point cannot always be 
decided. Fractures inflicted duiTng life are. as a rule, attended with 
more extravasation of blood and evidences of reaction in the sur- 
rounding tissues : but fractures produced within a few hours after 
death may resemble these very closely. Usually a greater degi'ee of 
force is necessarv to fracture bones in the dead than in the h^-ins: 
body. 

Scars and Tattoo JIarks. — The presence and character of cica- 
trices should be noticed. Scars produced by any considerable loss of 



POST-MORTEM EXAMINATIONS. 9 

substance may become very much smaller and less conspicuous, but 
never entirely disappear. Slight and superficial wounds, however, 
produce marks which may not be permanent. The discoloration 
produced by tattooing may, although rarely, disappear during life. 

INTERNAL EXAMINATION.' 

After completing the external inspection of the body we com- 
mence the internal examination. In order that this examination 
may be made both thoroughly and rapidly, we should follow a regular 
method. The method should be such as will enable us to examine 
the relations of parts to one another, without seriously disturbing 
them, and to remove and inspect the organs in such an order and 
manner as will not interfere with the examination of parts which 
are to follow. In certain cases it may be necessary to depart from 
the regular method ; but, as a rule, the following plan will be found 
most advantageous. 

It is important to remember the difference between the distribu- 
tion of the blood in the body during life and after death. During 
life the blood is in constant motion and is distributed in a regular 
way in the heart, capillaries, arteries, and veins. Inflammations and 
obstructions to the circulation may disturb this natural distribution 
and produce congestion of particular parts of the body. After 
death the blood ceases to circulate ; it leaves the left cavities of the 
heart, the arteries and capillaries, and collects in the veins and the 
right cavities of the heart. According to the character of the dis- 
ease which causes death, coagulation of the blood takes place more 
or less extensively and at an earlier or later period. The local con- 
gestions which existed during life often disappear after death. On 
the other hand, local congestions are found after death which did 
not exist during life. Thus, after death the scalp often contains a 
large amount of venous blood. The veins of the pia mater and the 
sinuses of the dura mater may be filled with blood. The mucous 
membrane of the larynx and trachea may appear to be deeply con- 
gested. The lungs are congested if the patient has been comatose 
for some hours before death. All the tissues of the back and the 
membranes of the spinal cord are often gorged with venous blood. 
The right auricle and ventricle of the heart may contain fluid or 
clotted blood in considerable quantity. 

THE HEAD. 

The scalp is divided by an incision across the vertex from ear to 



' Absolute and relative sizes and weights of various parts and organs of the body, 
and much other vaUiable statistical data, may be found in Vic'rordfs "Anatomische, 
Physiologische uud Physikalische Daten und Tabelleu," Jena, 188S. 



10 THE METHOD OF MAKING 

ear. The flaps are dissected forward and backward, taking up the 
temporal muscles with the skin and lea^-ing the pericranium at- 
tached to the bone. The internal surface of the scalp and the peri- 
cranium are to be searched for ecchvmoses and inflammatorv lesions. 
A circular incision is then made ^vith a saw, and the roof of the 
cranium removed. The incision in front should pass through a 
point about three and one-half inches above the bridge of the nose, 
behind through the occipital protuberance. "When the roof of the 
cranium is thus entirely loosened a stout hook is introduced under 
the upper edge of the calvarium, and this is wrenched off ^vith a 
jerk. 

Sometimes the dura mater is so adherent to the calvarimn that 
the latter cannot be torn from it without injury to the brain. In 
this case the dura mater may be cut through at the level of the 
cranial incision, and the brain removed 'v^'ith the calvarium and 
separated afterwards. Or, Avhich is better, after the circular in- 
cision has been made tlirough the bone, a longitudinal incision is 
made, from front to back, about three-quarters of an inch to one 
side of the median line of the skull, and a segment of bone removed. 
The knife blade may now be inserted from the open side, and the 
dura cut away from the skull cap along the line of the longitudinal 
sinus, where the adhesions are apt to be most firm. 

We should notice whether or not the calvarium is symmetrical. 
The cranial bones increase in size by a growth of bone at the edges 
of the sutures. If any suture become completely ossified and closed 
prematurely, the bones will be unequally developed. The thickness 
and density of the cranial bones vary considerably ^vithin the limits 
of health. There are often deep depressions on the inner surface of 
the skull along the sagittal suture, caused by the pressure of the 
Pacchionian bodies, and of no pathological significance. "We should 
observe the blood content of the bone, determine the existence or 
absence of fractures, inflammatory lesions, exostoses, etc. 

Tlie Dura Plater is now exposed to view. It will be found more 
or less adherent to the calvarium ; a moderate amount of adherence, 
especially in old persons, does not denote disease. Very extensive 
and firm adhesions are usually produced by inflammation, Xear the 
median line the Pacchionian bodies often project through the dura 
mater and may produce indentations in the internal surface of the 
calvarium. We must look for clots and for tumors and for inflam- 
matory lesions on the external surface of the dura mater. The 
longitudinal sinus should be laid open and its contents examined. A 
circular incision is then made through the dura mater in a line cor- 
responding to the cranial incision ; the f alx is di^-ided between the 
anterior lobes of the brain, and the entire membrane drawn back. 



POST-MORTEM EXAMINATIONS. 11 

We should observe the existence of abnormal adhesions of the dura 
mater to the pia mater, bearing in mind that a moderate amount of 
adhesion along the longitudinal fissure is normal. The internal sur- 
face of the dura mater is to be examined for the products of inflam- 
mation and for tumors. 

The Pia Mater covering the convex surface of the brain is now 
exposed. The degree of congestion, and the existence of serum, pus, 
or blood, beneath, within, or upon it, are now to be ascertained 
before the brain is removed. The pia mater in old persons frequently 
loses its transparency and becomes thick and white ; this change 
is most marked along the longitudinal fissure and large vessels. 
Marked and general thickening of the pia mater is produced by 
chronic inflammation. Along the longitudinal fissure, and some- 
times at a considerable distance from it, we usually find small, ele- 
vated, whitish nodules, which are the Pacchionian bodies and are 
normal in the adult. 

The amount of serum beneath the pia mater varies. A consider- 
able amount, especially in cachectic persons, may exist without brain 
disease. Clear serum raising the pia mater and separating the con- 
volutions of the brain inay be simply dropsical or due to chronic 
meningitis. Turbid and purulent serum, beneath and in the pia 
mater, is produced by acute or chronic meningitis. The degree of 
flatness of the surface of the convolutions should be observed before 
removing the brain ; for, when marked, it affords an important indi- 
cation of pressure, from haemorrhage, inflammatory products, inter- 
nal fluid effusions, and tumors. The pia mater should be carefully 
examined for miliary tubercles. 

The Brain, — -After examining the convex surface of the brain 
the anterior lobes of the cerebrum are to be pulled gently backward, 
the nerves, vessels, and tentorium severed, and the medulla cut 
across as low down as possible. The brain is now removed from the 
cranium by passing the fingers of one hand down, beneath and 
behind the lobes of the cerebellum, and drawing the brain out, sup- 
porting the convexity with the other hand. 

The adult brain in the male weighs on the average about 1,400 
gm. (49^ oz.); that of the female, about 155 gni. (5 oz.) less. The ave- 
rage proportional weight of the brain to that of the body is about one- 
forty-fifth, although in this, as in the absolute weight, there is 
considerable variation. 

The exact situation of any lesion which is apparent externally 
should be described by its relation to the lobes, fissures, convolu- 
tions, and sulci. 

The brain is first laid upon its convex surface, and the anterior, 
middle, and posterior cerebral arteries, as well as the basilar and the 



12 



THE METHOD OF MAKING 



carotids, are to be examined for emboli, thrombi, atheroma, and 
aneurisms. Evidence of extravasations of blood, tumors, and 
inflammatory lesions are now to be looked for. The brain is next 
turned over on to its base. An incision is made through the pia 
mater over the convex surface of the cerebrum. The membrane is 
stripped up, and its adherence to the brain and its thickness noted. 

The more common method of opening the brain is as follows : 
. The halves of the cerebrum are to be separated until the superior 
surface of the corpus callosum is exposed. A longitudinal incision 
is made through the junction of the corpus callosum and the cere- 
brum, and downward into the ventricle. The incision should be 



iAitaV 




Fig. 1.— Side View of the Human Brain, sHowiNa its Fissures and Convolutions. 



made carefully, so as not to cut through the ventricle into the gan- 
gha below. The incision thus made through the roof of the ventricle 
is prolonged back^vard and forward in the direction of the cornua, so 
as to expose the entire ventricle. A longitudinal incision is then 
made outward and backward into the hemisphere, from the outer 
edge of the lateral ventricle, nearly to the pia mater. A second 
incision is then made through this cut surface out'ward, and this is 
repeated until the hemisphere is divided into a number of long, 
prism-shaped pieces, held together by the pia mater and a small por- 
tion of the cortex. The brain is now turned around so as to bring 
the other hemisphere under the hand, and the operation is repeated 
on the other side. 



POST-MORTEM EXAMINATIONS. 13 

The size, shape, and contents of the ventricles should be noticed, 
and the thickness and appearance of the ependyma. 

The fornix and the central portion of the corpus callosum are cut 
across by passing the point of the knife through the foramen of 
Munro and cutting upward. They are then drawn backward, one 
of the posterior cornua of the fornix being severed and laid to one 
side. The velum interpositum and the choroid plexus are now dis- 
sected up, the blood contents and the general appearance noted, and 
the third ventricle examined. Not infrequently small cysts of the 
choroid are found, which seem to have little or no pathological 
significance. 

The fourth ventricle is now opened by a longitudinal incision 
through the vermiform process. Each hemisphere of the cerebellum 
is divided first into two parts by an incision through the upper and 
inner convex border, and then each segment is further divided by 
incisions in the same direction. 

Thin transverse sections are now made through the cerebral 
ganglia, commencing in front. The ganglia are supported, and the 
sections caused to fall apart as they are cut, by carrying the fingers 
of one hand under the brain, and gently lifting the ganglia at points 
just beneath where the sections are made. It is important to observe 
the exact position of any lesion which may be discovered in the cere- 
bral ganglia, their relations to the external and internal capsule and 
to the caudate and lenticular nucleus. 

Finally the segments of the cerebrum and cerebellum are folded 
up together into their original positions, the whole is turned over on 
to the vertex, and thin sections are made through the medulla. 
Small clots in the medulla should not be overlooked. 

In case of the discovery of apoplectic clots, areas of softening, 
etc. , either in the hemispheres or in the basal ganglia, after their 
location and extent are determined they should be carefully searched 
for lesions of the blood vessels, minute aneurisms, areas of degenera- 
tion, and ruptures. For this purpose it may be necessary to allow a 
stream of water to run over the affected portion, so as to wash out 
the brain substance and expose the vessels. In some cases the blood 
vessels are best exposed by macerating the brain tissue at the seat of 
the lesion for some hours in water, and then washing out the brain 
substance under the faucet. 

While the above mode of dissecting the brain gives a very com- 
plete view of the seat and extent of lesions in general, where a more 
exact localization of lesions with a microscopical examination is to be 
made the following is a better method of opening the brain : 

After completing the external examination, as detailed above, the 
brain is laid on its vertex, the cerebellar end toward the ojierator. 



14 



THE METHOD OF MAKING 



The cerebellum is raised by the fingers of the left hand, and the pia 
cut through along the sides of the corpora quadrigemina and along 
the inner margin of the temporal lobes to the middle cerebral artery 
on both sides. Then, raising the temporal lobes, in turn, by their 
apices, the pia is cut through along the course of the middle cerebral 
artery into the Sylvian fissure, and along the course of its posterior 
branch to its end. ^ow drawing the temporal lobes one after the 
other upward and outward, their junction with the base is cut, the 
knife being held horizontally so as not to injure the basal ganglia, 
until the descending horn is opened. The point of the knife being in 
the descending cornua, the incision through the brain substance then 
passes outward and backward well into the posterior cornua, thus 
partially severing, at the lateral surface of the brain, the junction of 
the occipital and temporal lobes. The temporal lobes are then turned 
outward and backward (Fig. 2). 




Fig. 2. — Vie"w of the Base of the Brain, with the Temporal Lobes turned Backward 
-A.ND Outward. 

A B, line of transverse incision. 

The operculum is now pulled well outward, completely exposing 
the island of Reil, and a slightly curved transverse incision is made, 
deep enough to pass into the anterior horns of the ventricles, connect- 
ing the anterior sulci of the island of Reil (Fig. 2, A, B). ■ 

i^ow raising the cerebellum and inserting the point of the knife 
into the ventricle, with short incisions from "svithin outward cut 
through the internal capsule on either side from back to front, care 
being taken not to injure the basal ganglia. Then cut across the 
crura of the fornix and the septum lucidum, lea^dng the fornix lying 
on the corpus callosum. 

The square basal piece thus freed — the brain axis — includes the 



POST-MORTEM EXAMINATIONS. 



15 



island of Reil, the basal ganglia, the crura, pons, medulla, and cere- 
bellum (Fig.)3. 

The remaining portion — the brain mantle — includes the convolu- 
tions, corpus callosum, and fornix. 

The basal piece may be further examined by a series of trans- 
verse incisions from one-half to three-quarters of an inch apart, and 
it may then be hardened either with or without the cerebellum. The 
convolutions may be cut into small pieces by longitudinal and trans- 
verse incisions, made from within and not reaching quite to the pia 
mater, which will then serve to hold the pieces together in their 
proper relations to one another. ^ 

For the methods of hardening and preserving the brain tissues, 
see p. 16. 

The Base of the Cranium, — We now return to the skull. The 
remaining sinuses of the dura mater should be opened, and this 




Fig. 3.— Drawing of the Brain Axis, separated from the Brain Mantle, as seen from 

ABOVE. 

membrane then entirely stripped from the bone. The bones at the 
base of the skull are to be examined for fractures, inflammatory 
lesions, and tumors. In cases of acute purulent meningitis the 
temporal and frontal bones should be carefully examined, as the 
inflammatory process is sometimes transmitted from the internal ear, 
or mastoid cells, or frontal sinuses. 

The eyes may be removed by breaking the roof of the orbit with 
a hammer, removing the fragments of bone, and dissecting away 
bone and muscles, so as to expose the optic nerve and posterior 
segment of the eye. That portion of the globe which is not covered 

^ For further details of this method of opening the brain and a consideration of 
its advantages, see Van Gkson, New York Medical Journal, July 20th, 1SS9. 



16 THE METHOD OF MAKING 

by conjunctiva can now be cut away with scissors and removed with 
the optic nerve, or, when permissible, the whole eye may be cut out. 

Hardening and Preservation of the Tissues for Microscopical Examination. — For 
the study of tumors and inflammatory lesions of the bones of the skull and ossifica- 
tions of the dura mater and pia mater, the affected portions should be cut into small 
pieces, decalcified, and subsequently hardened in strong alcohol. In the ordinary 
lesions of the dura mater, the tissues are best hardened and preserved by stretching- 
the diseased portions on a flat piece of wood or cork with pins, and placing them in 
Muller's fluid. ^ 

The pia mater is so delicate that if it be torn from the brain when quite fresh its 
tissues are apt to be injured. The portions of the pia mater which are to be preserved 
should therefore be removed by cutting off slices of the brain substance about 
half an inch thick, with the membrane still attached, and placing the whole in 
Mliller's fluid. After twenty-four hours the pia mater will have become sufficiently 
hard to permit of its being stripped off without injury, and it is then spread loosely 
on a flat cork with pins, the free surface outward, and the cork floated, specimen side 
down, in a dish of alcohol (eighty per cent). The next day strong alcohol may be 
used, and the hardening is complete in three or four days. The pia mater should 
not remain longer than twenty- four hours in Mliller's fluid before being stripped off, 
for after this time it usually becomes so firmly attached to the brain substance as to 
render its removal very diflicult. 

The ependyma, when this alone is to be studied, maybe sliced off with a suflacient 
quantity of underlying brain substance to prevent its folding, and hardened in 
Mliller's fluid. Special care should be exercised not to touch the surface of the 
ependyma, since the epithelium is easily rubbed off. 

The brain substance, after having been cut into sufficiently small pieces for the 
general examination, should be hardened in Mliller's fluid. Large quantities of the 
fluid should be used, four or five times the bulk of the tissue, and the pieces of tissue 
should either be suspended in gauze or kept apart by a little absorbent cotton. The 
fluid should be kept cool, and changed on the second, fifth, and eighth days, and 
again in the third week. 

In general, two or three months are required to secure a good hardening with 
Mliller's fluid. When the hardening is complete the brain tissue is rinsed off with 
water and put in eighty- per-cent alcohol, in which it may be kept, preferably in the 
dark. 

Great care is required in hardening and preserving nerve tissues, and most of the 
ordinarily practised methods give only caricatures and gross distortions of the brain 
structure. 

Too long a soaking in Mliller's fluid renders brain tissue very brittle. To get the 
best hardening the single pieces ought not to be larger than 1 c.c. 

When, for topographical purposes, large pieces of the brain are to be preserved, it 
is well to add one sixth of its bulk of alcohol to the Mliller's fluid to aid its penetra- 
tion. 

Certain lesions, particularly the softenings of the brain, are best studied by teas- 
ing, when fresh, in one-half-per-cent solution of sodium chloride, or in frozen sections 
of the fresh tissue. (See chapter on the Nervous System.) The blood vessels should 
be stretched on cork with pins and hardened with Mliller's fluid and alcohol. The 



1 For the details of the methods of hardening, decalcifying, staining, etc., see the 
end of Part I. 



POST-MOKTEM EXAMINATIONS. 17 

eye and portion of the optic nerve, if removed, should be hardened with Milller's 
fluid. 1 

THE SPINAL CORD. 

The examination of the spinal cord is usually most conveniently 
made after the removal of the brain. 

The body should be placed face downward, with a block under 
the thorax and the head hanging over the edge of the table. An in- 
cision is made through the skin and muscles along the entire length 
of the spine, and the soft parts dissected away on each side so as to 
expose the laminae of the vertebral column. The laminae are then 
divided close within the articular processes with the saw. 

The saw should be so directed in severing the laminae that the in- 
cision shall touch the outer border of the spinal canal, as otherwise 
the laminae and spinous processes are not easily separated. 

Great care should be taken on the one hand not to injure the cord 
with saw, and on the other to completely loosen the portions of bone 
to be removed. These, which are the spinous processes and laminae, 
are now torn away together with a stout hook, exposing the cord. 

By means of a long, curved chisel, made for this purpose, the 
bodies of the vertebrae may be removed from the front after the tho- 
racic and abdominal viscera are taken out, and the cord thus exposed 
and removed. 

But in this anterior method of removing the cord, as well as by 
the use of chisel and mallet, bone shears, etc., in the ordinary method, 
there is great liability of injuring the delicate tissues of the cord and 
producing, asVanGieson has shown, ^ mechanical alterations which 
are liable to be mistaken for malformations or the effects of disease. 

When the body has lain on the back, the membranes of the cord 
may be found considerably congested without indicating the pre-ex- 
istence of any disease. If the body has lain for some time, especially 
in warm weather, serous fluid may have accumulated within the 
membranes as a result of post-mortem change. 

The roots of the nerves are now to be cut across, as far away as 
possible from the cord, and the cord removed in its membranes, care 
being taken not to press it in any way. It is the safest plan not to 
grasp the cord itself, but with a forceps to seize the dura mater and 
thus lift it up at once as it is freed from its attachments. It is now 
laid on the table, and the dura mater laid open with scissors on the 
anterior and posterior surfaces over its entire length, and searched 
for tumors, inflammatory lesions, etc. The finger should be passed 
gently along the cord as it lies on the table, so as to detect any 

^ For the details of the methods of hardening, decalcifying, staining, etc., see the 
end of Part I. 

2 Va7i Oieson, New York Medical Journal, 1893. 
2 



18 THE METHOD OF MAKING 

marked softening or sclerosis. It should now be held lightly over 
the fingers, and smooth transverse incisions made, with a very 
sharp knife or razor, about half an inch apart through its entire sub- 
stance, leaving the segments attached to the pia mater. The cut 
surfaces should be carefully examined for abnormal blood contents, 
haemorrhages, inflammatory lesions, softening, scleroses, and pigmen- 
tations. Important lesion of the cord may be invisible to the naked 
eye, and hence, if disease be suspected, the organ should be pre- 
served for microscopical examination. After removal of the eord 
fractures and displacements of the vertebrae are easily recognized. 

Preservation of the Spinal Gord and its Membranes, and of Peripheral Nerves. — 
After the removal of the spinal dura, the entire cord with its nerve roots — the seg- 
ments into which it has been cut for gross examination being left in place — should 
be laid on a wad of absorbent cotton in a large jar of Miiller's fluid, the segments be- 
ing slightly separated from each other by a little absorbent cotton. Yan Gieson 
recommends the careful rolling of the segmented cord into a loose spiral and lay- 
ing this coil on a wad of absorbent cotton in the Miiller's fluid. In this way the cut 
ends of the segments are held apart and accessible to the preservation fluid, and 
harden with little distortion. 

The hardening and preservation of the cord should be done by the same method 
as suggested above for the brain. The same care should be exercised as in the brain 
not to permit the cord to become brittle by remaining too long in the Miiller's fluid. 
If the dura mater of the cord alone is to be preserved, it should be treated in the 
manner suggested for the dura mater cerebralis. The pia mater spinalis is best 
studied in sections through the entire cord, the membranes being left in situ. 

Peripheral nerves may be hardened in Miiller's fluid, care being taken that they 
do not become brittle by too long soaking in it. The hardening is completed and 
the specimen preserved in alcohol. 

For the hardening of the peripheral nerves osmic acid is very useful, especially 
when changes in the myeline are to be sought after. 

As osmic acid does not readily penetrate the lamellar sheath so as to come in con- 
tact with the nerve fibres, in trunks of any considerable size, the following proce- 
dure as suggested by Yan Gieson will be found useful : A piece about one-half inch 
long is cut from the nerve to be examined, and, seizing one end of this segment with 
a forceps, with another forceps the individual nerve fibres, or small clusters of these, 
are pulled out of the lamellar sheath and put at once in one-per-cent aqueous solu- 
tion of osmic acid, in which they remain twenty-four hours, and are then washed 
and transferred to glycerin, to which twenty-five-per-cent alcohol is added. In this 
mixture they may be preserved. 

THE THORAX AND ABDOMEN. 

To examine these cavities the body is replaced on its back, and 
a single straight incision is made from the top of the sternum to the 
pubes, passing to the left of the umbilicus. For this purpose a large 
knife should be used, held firmly in the whole hand, and the move- 
ment should be mainly from the shoulder. The first incision should 
divide everything down to the sternum and peritoneum. A short 



POST-MORTEM EXAMINATIONS. 19 

incision should then be made through the peritoneum, just below the 
ensiform cartilage. Into this opening two fingers of the left hand 
are introduced and separated from one another, and, the parietes 
being raised and the sides of the opening being held apart by the 
fingers, the peritoneum is divided to the pubes, care being taken to 
hold the knife horizontally so as not to cut the intestines. The skin 
and muscles are then dissected off from the thorax on both sides as 
far back as the false ribs. 

This dissection should be made by long sweeps of the knife, which 
should be made to cut with the full blade and not with the point 
only ; and if the skin and muscles be pulled strongly away from the 
chest with the left hand, it may be done very rapidly and with a few 
strokes of the knife. We notice here the amount of subcutaneous 
fat and the condition of the muscles. In order better to expose the 
abdominal cavity, the rectus abdominis muscles should be divided 
transversely beneath the skin just above the pubes, and the abdomi- 
nal flaps may then be turned freely outward. 

General Inspection of the Abdominal Cavity. — We first notice 
the position and general condition of the viscera. It is best at this 
stage of the examination to note the condition of the vermiform 
appendix, and to look over the peritoneal cavity for serum, inflam- 
matory lesions, evidences of perforation, and for the existence of 
invagination, incarceration, and herniee of the intestines. A small 
quantity of reddish serum is frequently found in the abdominal 
cavity, particularly in warm weather, as the result of commencing 
decomposition. 

It should be remarked here that a variety of striking changes in 
the character and appearance of the internal organs are produced by 
putrefaction — changes which are often mistakenly regarded as evi- 
dences of disease, and much experience is required in judging 
correctly of their significance. These changes are, in general, soft- 
ening and discoloration, both of which may occur as the result of 
disease. It may be said in general that the post-mortem reddening 
or hypostases are most marked in the more dependent parts of the 
organs. Post-mortem softening usually affects entire organs, not 
being limited to a part as is often the case in disease. Gray or 
greenish-brown post-mortem discolorations are apt to appear in those 
organs or parts of organs which lie in contact with the intestinal 
canal. Parts of internal organs, such as the liver, which have been 
the seat of localized congestion during life, may after death take 
on a dark-greenish color. 

The omentum is usually spread over the surface of the small 
intestines, but it may be rolled up and displaced in a variety of ways, 
or may be adherent at some point to the small intestines or the 
abdominal wall. 



20 THE METHOD OF MAKING 

The surface of the small intestines should be smooth and shin- 
ing. They may be greath' distended ^vith gas, and thus so com- 
pletely cover the other abdominal ^^scera that it becomes necessary to 
let out some of the gas by a small puncture. The transverse colon 
passes across the abdomen through the upper part of the umbilical 
region. It may be lower than the umbilicus or higher up against 
the liver and diaphragm : it may be distended with gas or con- 
tracted. 

The liver is situated in the right hypochondiiac and epigastric 
regions, filling the conca^^ty of the diaphragm. Its upper border 
reaches, in the linea mammillaris, to the fifth intercostal space ; in 
the linea axillaris, to the seventh intercostal space ; close to the ver- 
tebral column, to the tenth intercostal space. At the median hne the 
upper border of the liver corresponds to the lower border of the 
heart. The left lobe extends about three inches to the left of the 
median line. The lower border of the right lobe usually reaches to 
the free border of the ribs, while the left lobe is ^4sible for about an 
inch below the ensiform cartilage. In women the liver is usually 
lower than in men. 

The position of the liver is affected by changes in the thoracic 
cavity, forcing it do^niward ; by changes in the abdominal cavity, 
forcing it upward ; by constriction of the waist in tight lacing, 
forcing it either upward or do^Tiward : by changes in the size of the 
organ itself. The liver may not only be displaced downward but 
dislocated, so that its convex surface faces the abdominal wall and 
its posterior edge is turned upward against the diaphragm. 

The stomach is situated in the left hypochondriac and epigastric 
regions, extending also into the right hypochondrium : it lies in part 
against the anterior wall of the abdomen, in part beneath the hver 
and diaphragm, and above the transverse colon. Its anterior surface, 
which is directed upward and forward, is in contact above with the 
diaphragm and the under surface of the hver, and lower down with 
the abdominal wall opposite to the epigastric region. Its posterior 
surface is turned downward and backward, and rests on the trans- 
verse mesocolon, the pancreas, and the great vessels. To its lesser 
curvature or upper border are attached the gastro-phrenic ligament 
and the gastro-hepatic omentum. To the greater curvature or 
lower border is attached the gastro-colic omentum. Its cardiac 
orifice communicates ^vith the oesophagus, its pyloric end ^vith the 
duodenum. 

When the stomach is distended the greater curvature is elevated 
and carried forward, the anterior surface is turned upward and the 
posterior surface do^vnward. When distended with food or gas the 
organ is prominent ; when empty it may hardly be visible below 



POST-MORTEM EXAMINATIONS. 21 

the ribs ; when the intestines are dilated it may be entirely covered 
loy them. 

Before opening the thorax the hand should be passed up against 
the under surface of the diaphragm on either side to determine its 
height. According to Quain, the vault of the diaphragm rises, in 
the dead body, on the right side to the level of the junction of the 
fifth rib and sternum, on the left side as high as the sixth rib. Both 
the relative and the absolute height of the diaphragm vary under a 
variety of pathological conditions. 

If the existence of air or gas in the pleural cavities be suspected, 
the abdominal cavity should be filled with water and the diaphragm 
punctured below the level of the fluid. If air be present it will 
escape in bubbles through the water. 

THE THORAX. 

We now leave the abdominal viscera and proceed to the exami- 
nation of the thorax. With a costatome or a strong knife the 
costal cartilages are divided close to the ribs, the clavicles are dis- 
articulated from the sternum, and the latter removed, taking care 
not to wound the large veins. We first examine the position of 
the heart and lungs. 

The Heart. — The upper border of the heart is on a level w^ith the 
third costal cartilage ; the lower border extends from 1.3 cm. (^ in.) 
below the lower end of the sternum to the fifth left intercostal space. 
The left boundary of the heart is situated to the left of the junction 
of the fifth rib with its costal cartilage, and behind or to the left of a 
vertical line drawn downward from the left nipple. The right 
boundary extends about 2.5 cm. (1 in.) to the right of the right edge 
of the sternum. The portion of the heart uncovered by the lungs is 
of an irregular quadrangular shape. Its lateral diameter is from 
3.8 cm. to 11,1 cm. (11^-4^ inches); its upper boundary varies from 
the level of the second costal cartilage to that of the fifth, but it is 
usually behind the third or fourth cartilage or fourth space. 

The area of the heart which is found uncovered will, however, 
vary much accordiAg to the degree to which the lungs collapse after 
opening the chest. Any disease which diminishes the size of the 
lungs, or pleuritic adhesions which retract or bind them do^\ii, may 
increase the area of exposed heart. On the other hand, emphy- 
sema, pneumonia, or any disease which increases the size of, or re- 
tains the air in, the lungs, may diminish the area of exposed heart. 
The exposed area varies also with the size of the heart itself. 

The PericardiuDi is now opened by a slightly oblique incision on 
its anterior surface. The existence of serous, fibrinous, or purulent 
exudation, and of adhesions, is to be noticed. A small quantity of 



22 THE METHOD OF MAKING 

clear serum exists normallj' in the pericardial sac, and this serum 
may be blood-stained from beginning decomposition. White thick- 
enings of the pericardium on the surfaces of the heart are often seen; 
they do not indicate important disease. 

Now that the pericardial sac is open, the position of the heart can 
be clearly seen. It lies obliquely in the chest, its long axis at an 
angle of about 60 degrees with that of the thorax. The portion of 
the heart which is first seen is the anterior surface of the right ven- 
tricle ; upward and to the right of this is the right auricle, which 
lies about two-thirds on the right of the sternum and about one-third 
behind it. Its upper border usually corresponds to the plane of the 
middle of the anterior end of the second intercostal space on the 
right side. Its size varies with the amount of blood which it con- 
tains. The left auricle lies behind the root of the pulmonary artery, 
so that only its appendix is visible. The middle of the auricle cor- 
responds to the third costal cartilage. Of the left ventricle only a 
narrow rim is seen, on the left side of the right ventricle. The pul- 
monary valve is usually entirely or in part on the left side of the 
sternum, behind the second space or third costal cartilage. 

The aortic valve is usually at the level of the third cartilage or 
the third space, and behind the left two- thirds or half of the sternum. 
The mitral valve is oblique, the upper end to the left. It is on the 
level of the third to the fourth cartilage, near the middle of the 
sternum. The tricuspid is oblique, its upper end to the left : the 
upper end is at the level of the third cartilage, the third space, or the 
fourth cartilage. The valve is opposite the middle of the sternum. 

The hand should now be passed over the arch of the aorta, to 
ascertain whether or not an aneurism is present. The heart is then 
grasped at the apex, raised out of the pericardium, tilted upward, 
and removed unopened by cutting through the vessels at its base. 

To determine the sufficiency of the aortic and pulmonary valves, 
the heart is held horizontally by both auricles, so as not to pull the 
valves open, and water is poured into the aortic and pulmonary arte- 
ries, and we observe how well the valves support the column of 
liquid. To ascertain the sufficiency of the mitral and tricuspid valves^ 
the auricles are first laid open so as to expose the upper surfaces of 
the valves. A large pipe is passed through the aorta or pulmonary 
artery beyond their valves, and a small stream of water allowed to 
flow into the ventricles. The auriculo- ventricular valves tv411 be 
swollen upward, and we can observe their degree of sufficiency. The 
tricuspid valve is normally somewhat insufficient. These water 
tests, however carefully applied, are not very reliable, since under 
the most favorable conditions the natural bearings of the valves are 
not perfectly preserved. 



POST-MORTEM EXAMINATIONS. 23 

To ascertain the size of the different valvular openings, we intro- 
duce the fingers, held flat with their sides in contact, into each of the 
orifices, and then measure the width of the fingers at the point where 
they fill the orifice. In this way we find that, under normal condi- 
tions in the adult, the aortic orifice measures about 2.5 cm. (1 in.), 
the mitral valve about 4.5 cm. (1.8 in.), the pulmonary about 3.1 cm. 
(1.2 in.), the tricuspid about 5 cm. (2 in.). 

In order to examine the interior of the heart, we first make an 
incision through the anterior wall of the right ventricle, close to the 
septum, and reaching to the apex of the ventricle ; through this open- 
ing the blade of the enterotome is passed into the pulmonary artery 
and the ventricle and artery laid open. With a little care the in- 
cision may be made to pass through one of the points of junction of 
the valves. 

The auricles and ventricles may be empty, or may contain fluid 
blood or the so-called heart clots. These heart clots are of two kinds 
— those which are formed some time before death, and those which 
are formed during the last hours of life and after death. The clots 
which are formed some time before death are usually associated with 
organic disease of the heart, especially with dilatation of the ventri- 
cles. They are firm, dry, and of whitish color ; they may soften or 
be infiltrated with the salts of lime. They are free in the cavities of 
the heart, or entangled in the trabeculse, or firmly adherent to the 
endocardium. They are composed of coagulated fibrin, or, rarely, of 
sarcomatous tissue as a complication of sarcoma in other parts of the 
body. The clots which are formed during the last hours of life and 
after death are red, yellow, or white. They may be soft or succu- 
lent, or quite firm. They may be free in the heart cavities, or be 
adherent to the trabeculse, or extend into the large vessels. They 
are usually most constant and of largest size in the right auricle and 
ventricle. Such clots may be formed within two hours after death. 
Clots of this character are a regular post-mortem condition and of 
no pathological significance. It is evident, however, if the blood did 
coagulate in the heart within twenty-four hours before death, that 
this coagulum could not be distinguished from the ordinary post- 
mortem clots. If it is supposed, therefore, that a person dies from 
heart clot developed a few hours before death, the proof of this must 
be derived largely from the clinical symptoms and not from the 
autopsy. 

The condition of the pulmonary valves and of the endocardium, 
and the thickness and appearance of the walls of the ventricle, are 
now noticed ; the left ventricle is opened by an incision through its 
anterior wall, close to the septum, and examined in the same way. 
We sometimes see the endocardium of the upper part of the left veu- 



24z THE METHOD OF MAKIXG 

tricle thick and white without the existence of valvular lesions or 
any clinical history of disease. The endocardium and valves are 
often stained red, particularly in warm weather, by imbibition of 
coloring matter of the blood set free by decomj^osition. To complete 
the examination of the cavities the enterotome is passed into each 
auricle, carried doAvn into the corresponding A-entricle, and an in- 
cision made along the outer border of both aiu-icle and ventricle to 
the apex of the latter. In this way the auricido- ventricular valves 
are completely exposed. 

After removing the blood the heart should be finally weighed. 
In adults the normal average weight of the heart is about 337 gm. 
(about I'i oz. ). The relative weight of the heart to that of the body 
is in males about 1 : 15S-17S ; in females, about 1 : 149-176. Ac- 
cording to Buhl, the average thickness of the wall of the left ven- 
tricle at about the middle of the cavity is from 1.6 cm. to 1.7 cm. 
(from about f to f in. ) ; of the right ventricle, from 0.4 to 0.6 cm. 
(from about ^ to ^ in. ) . 

Generally speaking, the size of the heart corresponds to the size 
and the development of the indiA-idual. In judging of an increase 
or decrease in its size we must consider the weight of the organ and 
the thickness of its walls. If the j^erson die while the heart is con- 
tracted, the walls of the ventricles "will appear thicker, their ca^-ities 
smaller than usual. If he die of some exhaustmg disease, hke 
tyi^hoid fever, or if decomposition have commenced, the heart walls 
aWU usually be flabby and the cavities will appear larger than usual. 

Preservation of Specimens. — Parenchyraatous and fatty degeneration of the heart 
muscle are best studied microscopically by teasing the fresh muscle in one-half-per- 
cent salt solution, or by examining in the same solution fresh sections made 'ffiththe 
freezing microtome. For the study of interstitial changes, fatty infiltration, etc., 
small pieces of the heart muscle should be hardened in Mliller's fluid. The yalyes 
may be stretched on a flat cork yrith pins, laid for forty-eight hours in a mixture of 
equal parts of one-sixth-per-cent chromic acid and alcohol, and then transferred to 
strong alcohol. For the methods of detecting bacteria in ulceratiye endocarditis, 
see section on Bacteria Stairing. When the presence of bacteria is suspected the 
specimen should be preserved in strong alcohol. 

The Pleural Cavities are next examined. The hand is passed 
into each, and the existence of serous or fibrinous exudations or of 
old adhesions ascertained. The method of detecting the presence of 
air has been given above. After the commencement of putrefaction 
reddish serum may accumulate in the pleural cavities. This should 
not be mistaken for the result of disease. 

The Lungs. — Each lung is lifted up in tirni, the vessels, etc., at 
its base diA^ided, and the organ removed. If the pleura is very 
adherent it is better to strip off the costal pleura Avith the lung. 



POST-MORTEM EXAMINATIONS. 25 

After inspecting the external surface of the lung, observing its size, 
shape, color, and consistence, we open the bronchi. For this purpose 
yve use scissors with long, narrow, blunt-pointecl blades, one blade a 
little longer than the other. The lung is held in the left hand with 
its base upward. We first open the large bronchi which run on the 
inner side of the lower lobe, afterward those of the upper lobe. 
Each bronchus should be followed to its smaller ramifications. 

We should observe the contents of the bronchi and the appear- 
ance of their walls. In the larger and medium-size bronchi the car- 
tilages in their walls do not form complete rings, but appear shining 
through the mucous membrane like irregular white patches. This 
ajDpearance should not be mistaken for a pathological change. In 
bodies which have been dead for some time, especially in cold 
weather, the bronchial mucous membrane may be red and swollen 
as a post-mortem change. The contents of the stomach are some- 
times forced, after death, into the pharynx, and thence find their way 
into the trachea and bronchi, giving them a peculiar reddish and 
even gangrenous appearance. Bronchitis does not always leave 
lesions which can be seen after death. 

After the examination of the bronchi the lung is turned over, the 
vessels, etc. , at its root grasped with the left hand, and a long, deep 
incision made from apex to base. We observe the appearance and 
texture of the lungs, whether the air vesicles are dilated (einphy- 
sematous) or filled with serum, blood, or inflammatory exudation. 
Fluid can be pressed out of the air vesicles without breaking down 
the lung tissue. Solid inflammatory exudation, on the other hand, 
renders the lung more resistant and easily broken down. Attention 
should be paid to the oozing of purulent or other fluid from the 
smaller bronchi when the lung is squeezed near thq^ cut surface. It 
is the rule to find the lower lobes more congested than the upper. 

Preservation of the Lungs and Bronclii, — If the lungs have been cut, small pieces 
from the affected portions of lung tissue or bronchi should be hardened in Miiller's 
fluid, care being taken not to squeeze or handle them unnecessarily. It is better, 
when the microscopical examination is more important than the macroscopical, not 
to open the lungs at once, but to fill the air spaces with preservative fluid by means 
of a funnel attached to a short rubber tube and canula, which is tied into the main 
bronchus. In this way not only are the minute structures preserved better, but the 
air vesicles are filled out and hardened in an approximately natural condition. Care 
should be taken not to have too great a pressure from the inflowing fluid, since then 
exudations might be displaced or the lung distorted or ruptured. While the lung is 
being filled it should be immersed in a vessel of the same preservative fluid, in 
which it lies for twenty-four hours. It is then cut into small pieces and the harden- 
ing completed. A variety of hardening agents may be used : Miiller's fluid, strong 
alcohol, or the mixture of equal parts of one-sixth-per-cent solution of chromic acid 
and alcohol. For general purposes the latter fluid is perhaps the best. If. however, 
the lung is commencing to decay, strong alcohol will stop the process more quickly 



26 THE METHOD OF MAKING 

and give as good results as are possible under the circumstances. Alcohol should be 
used when the lungs are to be examined for bacteria. 

It is often desirable, and particularly in cases in which the topography of lesions 
is to be studied, as in acute miliary tuberculosis, acute and chronic phthisis, infarc- 
tions, etc.. to inject the blood vessels with colored gelatin. The lung should, after 
the iniection, be hardened in alcohol. 

The Pharynx, Larynx, CEsophagus, and Thyroid Gland. — For 
the removal of these parts the incision through the skin should be 
carried upward as far as practicable — when allowable, to a point 
one inch below the chin, the head being allowed to hang backward 
over the edge of the table. 

The soft parts are dissected from the larynx, taking care not to 
cut the thyroid body, and an incision is made through the floor of 
the mouth, following the internal surface of the inferior maxilla. 
Through this incision the fingers are introduced into the mouth, the 
tongue drawn do^vn, the posterior wall of the pharynx divided above 
the tonsils, and the pharynx and larynx drawn out together. These 
organs are then pulled downward, and with the aid of the knife the 
ti'achea and oesophagus are removed entire, the oesophagus being cut 
just above the stomach. If the contents of the stomach are to be 
preserved, as in cases of suspected poisoning, a ligature is put 
around the oesophagus just below the point at which it is to be cut 
off. 

With the enterotome the pharynx and oesophagus are now slit 
open upon their posterior surfaces. The mucous membrane thus 
exposed is examined for evidences of caustic poisons, of inflamma- 
tion, tumors, strictures, etc. The enterotome is next introduced into 
the larynx, and this organ and the trachea laid open along the poste- 
rior wall. Here we look for oedema of the aryteno-epiglottidean 
folds (oedema of the glottis), for evidences of catarrhal, croupous, 
ulcerative, and syphilitic inflammation, and for tamors and lesions 
of the larjTigeal cartilages. CEiema and redness of the larynx 
may be produced by post-mortem changes, especially in bodies 
which have been kept for several days in cold weather. A well- 
marked oedema glottidis during life may leave no trace after death. 
Putrefactive chansfes usuallv commence earlv in the lar^-nx and tra- 
chea. 

The thyroid gland is dissected off and examined. Its weight 
varies a good deal, being, according to Krause, somewhat over 30 
gm. (about 1^ oz.). 

Preservation of the Larynx, Trachea, etc. — The larynx and trachea are freed from 
superfluous tissue and suspended entire by a thread in a large quantity of a mixture 
of equal parts of one-sixth-per-cent chromic acid and alcohol. The mixture should 
be renewed at the end of twenty-four hours, and again on the third and sixth days ; 



POST-MORTEM EXAMINATIONS. 27 

at the end of ten days the specimen is washed and transferred to strong alcohol, in 
which it is preserved. The oesophagus should be stretched on a flat cork with pins, 
and then treated in the same way. For bacterial study the specimens should be 
preserved in alcohol. The thyroid may be cut into small pieces and hardened either 
in Mliller's fluid or alcohol. 

THE ABDOMEN. 

Returning now to the abdominal cavity, we first dissect off the 
omentum. If tubercles of the. peritoneum exist, they are best seen 
and studied in the omentum. The colon is then raised and dissected 
free, to the caecum on one side and to the rectum on the other. The 
colon and small intestines are then drawn first to the right and then 
to the left side, so as to expose in turn the right and left kidneys. 
As each kidney is brought into view an incision is made through 
the peritoneum over the track of the ureter. The ureter is followed 
through its entire length and its condition ascertained. 

The Kidneys are then removed, separating the peritoneum and 
fat from them with the hand, and dividing the vessels with the knife. 
The suprarenal capsules, which are attached to the upper end of 
each kidney, are removed at the same time. The kidneys may be 
softened by putrefaction, or the surface may have a greenish-gray 
color caused by the post-mortem action of putrefactive gases on the 
haemoglobin. 

An incision is made through the capsule, along the convex bor- 
der of the kidney, and the membrane stripped off. We notice the 
degree of adherence of the capsule to the kidney, and also the sur- 
face of the latter, whether smooth or roughened, pale, congested, or 
mottled ; an incision is made along the convex surface down to the 
pelvis, so that the organ is divided into halves. We observe the re- 
lative thickness of the cortical and pyramidal portions, as well as 
the size of the entire organ. To ascertain the latter point, it is well 
to weigh each kidney ; the normal weight is from 130 to 150 gm. 
(about 4|^ to 5 oz.). 

It is necessary to remember, however, that in a kidney which is 
much atrophied there may be an increase of fat in the pelvis, which 
gives the organ nearly its normal size and weight, while the kidney 
tissue proper may have in great measure disappeared. 

The weight of the kidneys of adults is given by Vierordt in gene- 
ral as about 0.48 per cent of that of the entire body. 

We now inspect the kidney tissue more closely, especially the 
cortical portion. The pyramids consist largely of tubes running in 
nearly straight lines from the apex to the base of each pyramid. 
These straight tubes pass from the pyramids into the cortex in 
bundles, called medullary rays, man}' of them retaining their straight 
course until they nearly reach the surface of the kidne}'. These 



28 THE METHOD OF MAKING 

straight tubules send off branches on all sides of the rays, which be- 
come convoluted, form Henle's loops, and Imally terminate in the 
glomeruli or Malphigian bodies. In this way the cortex of the kid- 
ney, as seen in section, is divided into alternate bands of straight 
tubes, convoluted tubes, and glomeruli ; both sets of bands being 
perpendicular to the surface of the kidney, and called respectively 
medullary rays and labyrinths. About the convoluted tubules and 
glomeruli is a rich venous plexus ; and since after death the blood 
usually remains in this plexus and in the glomeruli, the bands con- 
taining the convoluted tubules, i.e., the labyrinths, usually appear 
red, while the medullary rays are grayish-white. In a normal kid- 
ney, therefore, the cortex should be regularly striped in narrow al- 
ternating red and \vhitish bands. 

The average thickness of the . cortex of the kidney is about one- 
third of an inch. 

If there be extensive congestion the entire cortex is red. If the 
epithelium of the tubules degenerates and fills them up, or if there 
are considerable changes in the interstitial tissue, the regular bands 
are lost and the cortex is irregularly mottled. If the tubular epithe- 
lium becomes filled with fat globules, this is indicated by an opaque 
yellow color of the affected parts ; in many cases, therefore, the ex- 
istence of kidney disease can be recognized with the naked eye. 

If waxy degeneration be present to a marked extent, it may be 
manifest by a peculiar translucent appearance of the affected parts, 
but in most cases it is necessary to apply reagents to demonstrate it 
satisfactorily. The cut surface of the kidney is washed with water 
to free it from blood, and repeatedly brushed with an aqueous solu- 
tion of iodine (iodine 1 part, potassium iodide 3 parts, water 100 
parts). The glomeruli and the blood vessels are most frequently 
affected, and, if so, they will appear as mahogany-colored dots and 
lines on a yellow ground. 

The pelvis should be examined for inflammatory lesions and cal- 
culi. Sometimes a whitish fluid is seen in the pelvis and can be 
squeezed from the papillae ; this is produced by a post-mortem des- 
quamation of the epithelium, but is liable to be mistaken for pus. 

Preservation of the Kidney.— li the kidney be not opened the bloodvessels may be 
injected through the renal artery with alcohol ; or, which is better, after washing 
out the blood vessels with one-tifth-per-cent solution of chromic acid, the organ may 
be injected slowly under a low pressure with " Delajkld's osmic acid mixture" (see 
p. 49). 

After filling the kidney well with this solution, the ressels are tied and the entire 
organ placed in eighty- per-cent alcohol for twenty-four hours. It is then cut into 
^mall pieces and preserved in eighty-per cent alcohol. 

Instead of injecting the organ, small pieces may be cut out and hardened in the 



POST-MORTEM EXAMINATIONS. 29 

osmic acid mixture. This in most cases will be the routine practice, as the osmic 
acid is expensive and the operation of injection sonnewhat troublesome. 

Kidneys which are to be examined for the presence of bacteria should be cut into 
small pieces and placed at once in strong alcohol, which should be changed once or 
twice, and in which they are permanently preserved. 

The Suprarenal Capsules are in the foetus of an ovoidal, in the 
adult of a triangular shape. They are situated at the upper and 
inner border of the kidney, to which they are loosely attached by 
connective tissue. On the anterior surface is an irregular fissure, 
called the hilus, from which the veins emerge. The size varies con- 
siderably, but in the adult the average vertical diameter is from 3.2 
cm. (li in.) to 4.5 cm. (If in.), the transverse diameter about 3.2 cm. 
(li in.), and they are from 4.2 mm. {\ in.) to 6.4 mm. (i in.) in thick- 
ness. They weigh in the adult from about 4 gm. (1 3 ) to 8 gm. 
(2 3). They are composed of a cortical and medullary portion, the 
cortex forming a yellowish shell around the dark-red or brown me- 
dulla. They are enclosed in a connective-tissue capsule, from which 
fibrous processes extend inward, dividing the gland into a series of 
irregular chambers. Those in the cortex are mostly elongated, giv- 
ing this portion a striated appearance, while those in the medulla are 
polyhedral. It is in these spaces that the parenchyma cells lie. The 
suprarenal capsules readily decompose ; the inner layer of the cor- 
tex may soften and break down, so that the outer zone forms a sort 
of cyst filled with reddish-brown broken-down substance. Hyper- 
trophy, tuberculosis and cheesy degeneration, fatty degeneration, 
and tumors are to be looked for. 

Preservation. — The suprarenal capsules should be hardened in Miiller's fluid or in 
strong alcohol. 

The Spleen. — This organ has, when removed from the body, the 
general shape of a flattened ellipsoid, most curved on its external and 
posterior surface. It is situated in an oblique position on the left 
side of the stomach, and between its cardiac end and the diaphragm. 
The vessels are given off from its inner surface, which is crossed by 
a more or less well-marked vertical ridge. The point of emergence of 
the vessels is called the hilus. Its long diameter extends from the 
seventh intercostal space to the eleventh rib. Its upper portion is 
separated from the ribs by the lungs ; its lower portion by the dia- 
phragm. 

Its usual length in the adult is, according to Vierordt, from 12 \o 
13 cm. (about 4f to 5 in.) ; its breadth from 7 to 8 cm. (about 2f to 
3 in.); its thickness 3 cm. (about 1\ in.). Its average weight is 
about 171 gm. (about 7 oz.). The dimensions of the spleen as given 
by Krause are somewhat greater than the above. But its measure- 



30 THE METHOD OF MAKING 

ment and weight vary considerably within the hmits of health. It 
is in these respects the most variable organ in the body. In old age 
the average weight gradually diminishes. 

The spleen is enclosed in a fibrous capsule covered with perito- 
neum. The parenchyma is formed of blood vessels and fibrillar con- 
nective tissue, and of a soft, dark-red pulp in which are embedded 
whitish spheroidal or elongated bodies, the glomeruli or Malpighian 
bodies. In the normal human spleen the glomeruli are hardly per- 
ceptible to the naked eye, but sometimes they are ver}" plain. Some- 
times the fibrous stroma is very apparent, sometimes not. 

The size, consistence, and color of the organ vary a good deal 
without any known cause. Decomposition softens it. Thickenings 
of the capsule and abnormal adhesions are very common, and often 
occur without any clinical history indicating disease. We should 
look for changes in size, pigmentations, hyperplasia of the connec- 
tive tissue, amyloid degeneration, tubercles, and infarctions. 

!N'ot infrequently one or more spheroidal or flattened so-called ac- 
cessory spleens are found in the vicinity of the spleen ; they vary in 
size from that of a pea to that of a walnut. 

Preservation. — In certain diseases of the pulp, leukaemia, leucocythsemia, etc., the 
tissue should be teased, when fresh, in one-half -per- cent salt solution, or examined 
by the staining methods described under the lesions of the blood. For general pur- 
poses small pieces of the organ are hardened in Miiller's fluid. 

The Intestines. — The rectum is divided, the intestine seized 
with the left hand, and, being kept stretched, is separated from its 
attachments by repeated incisions through the mesentery close to 
the gut, until the duodenum is reached, where it is again cut off. 
The operation is more cleanly if, before dividing the gut, ligatures 
are placed around it at either end. The entire length of the gut 
is now laid open with the enterotome along the mesenteric attach- 
ment, the mucous membrane is cleaned with a stream of water and 
then examined. 

In cases of suspected poisoning a ligature should be placed 
around the rectal end of the gut and two around the duodenal end, 
and it is then cut off below the former and between the latter liga- 
tures. The gut is now opened and the contents emptied into a clean 
glass jar for delivery to the chemist, care being taken that they be 
not allowed to touch anything but the inner surface of the jar. 
After washing the intestine in pure fresh water and examining it, 
it should be placed entire in another clean jar and sealed. 

Cadaveric lividities are very common in the intestines, and are 
usually most marked in the dependent portions. They are apt to 
occur in patches, but may be diffuse and very extensive. If the 



POST-MORTEM EXAMINATIONS. 31 

wall of the gut be stretched they are often seen to be discontinuous, 
owing to the pressure of the blood from the parts which are squeezed 
by folds. Small patches of arborescent or diffuse red staining are 
often seen, formed by the imbibition from the vessels of decomposing 
haemoglobin. In the more advanced stages of decomposition the 
mucosa may be softened and loosened. A dark purple or brownish 
discoloration of the entire intestinal wall is frequently seen, either 
diffuse or in patches. Much experience and careful observation are 
requisite in forming a correct judgment regarding the significance 
of changes of color in the intestines. Caution is necessary in distin- 
guishing normal digestive hypergemia from abnormal congestion. 
A very considerable congestion may exist without disease. In chol- 
era seasons especially, observers are prone to call the most moderate 
degree of congestion abnormal. 

The lesions ordinarily to be looked for are catarrhal, croupous, 
and ulcerative inflammations, perforations, haemorrhages, strictures, 
tumors, amyloid degeneration, swelling and ulceration of the soli- 
tary follicles and Peyer's patches, and pigmentation. For the de- 
tection of amyloid degeneration of the mucosa this structure should 
be carefully washed and brushed with a solution of iodine (see p. 28). 

Presevoation. — For the general purposes of microscopic study portions of the gut 
should be gently stretched on cork (the mucosa side free) and placed for a few 
minutes in strong alcohol, and then transferred to eighty-per-cent alcohol, in which 
the hardening is completed. The transfer to weaker alcohol is to prevent the speci- 
men from becoming brittle. 

For obvious reasons the mucous membrane should be handled as little as possi- 
ble, for, in the majority of cases, decomposition and softening have already set in at 
the time of the autopsy, and, under the most favorable conditions, the epithelium is 
very easily rubbed of. 

In cases in which the most perfect preservation of the topographical features, as 
well as the minute structure of the intestinal mucosa, is desirable, even at the expense 
of an inspection of the fresh tissue, another mode of procedure is to be recommended. 

Selected segments of the gut are, after removal from the body, allowed to remain 
unopened on the table while ligatures are tied around the ends. The isolated seg- 
ments, or the whole gut, are now to be moderately filled — not distended — with strong 
alcohol by means of a syringe with a needle canula ; or one end of the segment 
may be tied and the alcohol introduced through a funneUit the other, which is then 
ligated. The segments to be preserved should now be placed unopened in strong 
alcohol. After twenty-four hours they may be opened with scissors or a sharp knife, 
cut into suitable pieces, and kept permanently in eighty-per-cent alcohol. Intes- 
tinal contents may be washed out with alcohol before filling the gut. 

The Stomach and Duodenum. — We now introduce the entero- 
tome into the duodenum at its transverse portion, and open it on 
the convex border. When the pylorus is reached the incision is 
carried obliquely over to the greater curvature of the stomach, along 
which it is extended as far as the oesophageal opening, and the organ 



32 THE METHOD OF MAKING 

examined in situ j or, if a more careful examination of the stomach 
is called for, after ascertaining whether or not the bile duct is per- 
vious (see below), the duodenum and stomach maybe removed to- 
gether, and the stomach opened and examined on the table. (If 
poisoning be suspected a ligature should have been placed, earlier in 
the examination (see above), around the lower end of the oesophagus 
and the duodenum. The stomach and duodenum are now removed 
together unopened. They are to be opened in a carefully cleansed 
glass jar, and after an inspection of the mucous membrane and the 
contents with the naked eye and a hand lens, stomach, duodenum, 
and contents are to be sealed in the jar for the chemist.) 

We now look for the orifice of the bile duct, which will be found 
about the middle of the descending portion of the duodenum on its 
concave border. Pressure on the gall bladder or on the common 
duct will usuall}^ cause the bile to flow into the intestine if the ducts 
are pervious. But a sufficient degree of stoppage may exist in the 
ducts to give rise to marked symptoms of disease without preventing 
the flow of bile under these conditions, even with a moderate pressure. 
A long director is now passed into the gall duct, which is laid com- 
pletely open ; ulcerations, cicatrices, gall stones, inflammatory le- 
sions, and tumors are looked for. In stricture of the gall duct the 
mucous membrane above will often be found bile-stained, while be- 
low it is colorless. At this point, should there be any special reason 
for doing so, the portal vein, which lies close behind the ductus cho- 
ledochus, should be opened and examined for periphlebitis, phlebitis, 
and thrombosis. The mucous membrane of the duodenum and sto- 
mach are now rinsed off and examined. Acute inflammations from 
caustic poisons, chronic catarrhal inflammations, haemorrhages, ul- 
cers, erosions, swelling of the solitary follicles (lymph nodules), and 
tumors are lesions most frequently seen. We sometimes find a dif- 
fuse congestion of the stomach similar to that produced by irritant 
poisons, as a result of doses of croton oil given just before death. 

Preservation. — The same methods should be used as for the intestines (see above). 
TumoTs should be cut into small pieces and hardened in Mtiller's fluid. 

The Liver. — To remove the liver, the diaphragm is first divided 
on one side of the suspensory ligament as far back as the spine ; the 
suspensory ligament is then divided ; then the right and left lobes 
being in turn raised, the lateral ligaments are severed. Then, seizing 
the left lobe, the organ is dragged obliquely downward into the ab- 
dominal cavity, the remaining attachments being dissected away. 
The liver is first laid on its superior surface and the gall bladder and 
its contents examined. The character of the gall is to be determined, 
and gall stones, inflammatory lesions, and tumors sought for. To 



POST-MORTEM EXAMINATIONS. 38 

determine the actual size of the organ, it should be both measured 
and weighed. Its size varies greatly in different healthy individuals, 
but in general it may be said that it measures from 25 to 30 cm. (10 
to 12 in.) transversely, from 15.3 to 18 cm. (6 to 7 in.) antero-poste- 
riorly, and about 9 cm. (3^ in. ) at its thickest part ; the ordinary 
bulk is about 229 to 252 c.c. (90 to 100 cu. in.) ; its ordinary weight 
between 1,550 to 1,860 gm. (50 to 60 oz.). In children its weight 
relative to that of the body is greater than in adults. The liver is 
increased in size and weight during digestion and by congestion 
from any cause. 

The surface of the liver is now examined, and it is then laid on 
its lower surface and several deep incisions made from the convex 
surface downward. The color and consistence of the liver tissue 
should be noticed, also the distinctness with which the lobular out- 
lines can be seen ; whether or not the centres of the lobules are con- 
gested or their peripheries lighter in color than usual ; the presence 
of tumors, tubercles, abscess, ecchinococcus, new connective tissue, 
and pigmentation. Suspected amyloid degeneration should be tested 
for by the iodine solution (p. 28). 

We often find the surface of the liver of a greenish or very dark- 
brown color ; less frequently the same color extends into the sub- 
stance of the organ. This discoloration, which is entirely post- 
mortem, is, like the similar discoloration of other internal organs, 
produced by the action of the gases or putrefaction on the coloring 
matter of the blood. 

PreservatiGn. — For the study of parenchymatous degeneration, sections of the 
fresh frozen tissue or small teased fragments should be examined in half-per-cent 
salt solution. For general purposes small pieces should be hardened in Miiller's 
fluid or in alcohol. Tumors should be treated in the same way. In many cases of 
marked cirrhosis the topography of the lesion is best demonstrated by injecting the 
organ with blue gelatin through the portal vein and then hardening in strong al- 
cohol. 

The Pancreas. — This organ, of a light yellowish-red color, is 
elongated, irregularly prismatic in shape, and flattened antero-pos- 
teriorly ; the right end, called the head, is broader than the rest 
and lies in the concavity of the duodenum. The remainder of the 
organ, the body and tail, are usually tapering and lie transversely 
in the abdominal cavity, the tail reaching to the spleen. Its size 
and weight vary considerably ; its usual length is from 15.3 to 20.3 
cm. (6 to 8 in.); its breadth about 3.8 cm. (14- in.); its thickness 
about 1.3 to 2.5 cm. (| to 1 in.); its weight is usually from TO to lOS 
gm. (2i to 3 J oz.). The organ may be rounded instead of flattened : 
the head and tail may be disproportionately large ; the tail may bo 
unusually long or may be divided or curved. The superior mesen- 
3 



34 THE METHOD OF MAKING 

teric artery and vein, which pass behind the gland, are usually partly 
embedded in it, but are sometimes completely enclosed. 

A longitudinal incision should be made through the whole gland, 
which raay remain in sifii, and its substance and duct should be 
searched for calculi, tumors, malformations, and evidences of acute 
and chronic inflammation, fat necrosis, and amyloid degeneration 
of the blood vessels. The pancreas is frequently of a dark-red color 
from post-mortem staining. 

Preservation. — Portions of this organ should be hardened in strong alcohol, and 
not in chromic salts, which destroy the gland cells. 

THE GEXITO-URIXARY ORGANS. 

The Male Organs, — If the urine is to be examined it may be 
drawn off with a catheter ; or a vertical incision may be made into 
the bladder just above the symphysis pubis, and some of the urine 
dipped out. The cut end of the rectum should now be grasped with 
the left hand and raised up, and this and the bladder, prostate 
gland, etc., dissected away from the pelvis, the knife being carried 
close to the bone. The bladder is now drawn backward and the 
loose tissue close under the symphysis pubis cut. The body of the 
penis is then shoved backward within the skin and dissected away 
from behind beneath the symphysis, and finally cut off just behind 
the glans penis. The penis and bladder are now drawn bactvvard 
and upward, and the pelvic organs removed together. Or, the penis 
may be removed by sawing away the bones above the pubic arch, 
and then dissecting away the penis, whose root is thus exposed. 

The pelvic organs are then laid on the table, the bladder upper- 
most ; a long director is passed into the urethra, which is opened on 
its upper surface through its entire length, and the bladder widely 
opened. In the urethra the presence of strictures, diverticulse, 
ulcers, inflammatory lesions is to be noticed ; in the bladder inflam- 
matory lesions, hypertrophies, congestion and ecchymosis of the 
mucous membrane, hyperplasia and ulcers of the lymph nodules, 
and tumors. The organs are now turned over ; the rectum opened 
and examined for varicose veins, haemorrhages, ulcers, strictures, 
and tumors. ^]iq prostate gland is then cut into and the presence 
of calculi, inflammatory lesions, hypertrophies, and tumors sought 
for. Lastly, the vesiciilce seminales are examined, in which, though 
rarely, we may find evidences of tubercular inflammation and dila- 
tation. 

The Testicles may be removed, when necessary, without cut- 
ting the scrotum, by enlarging the inguinal canals from within and 
crowding the glands through them and cutting them off. The 
average weight of the adult testicle ^vith its epididymis is, accord- 



POST-MORTEM EXAMINATIONS. 35 

ing to Krause, from 15 to 24.5 gm. (about from {- to f oz.) Inflam- 
matory lesions, tuberculosis, abscesses, and tumors are the most 
frequent lesions. 

Preservation. — The urethral canal and bladder may be pinned open and hardened 
in alcohol. The prostate, vesiculae seminales, testicles, and tumors should be hard- 
ened in Mliller's fluid or alcohol. 

The Female Organs. — The position and general condition of the 
pelvic organs should first be determined by inspection. Abnor- 
mal adhesions of the ovaries, broad ligaments, Fallopian tubes, and 
uterus ; malpositions of the uterus ; subserous tumors of the uterus, 
and ovarian tumors, are frequently observed. Heemorrhage into 
the posterior cul-de-sac is sometimes found. The urine should be 
collected, if necessary, as above directed ; the organs should be dis- 
sected away laterally, as in the male, care being taken not to injure 
the ovaries and Fallopian tubes. The bladder is then dra^vn strongly 
backward and upward, and dissected away from the symphysis and 
the pubic arch, and, the point of the knife being carried forward 
and downward, the vagina is cut off in its lower third, the rectum 
severed just above the anus, the remaining attachments cut, and 
the pelvic organs taken out together. If it be necessary to remove 
the external generative organs, after freeing the lateral surfaces of 
the internal organs and the bladder, the legs are widely separated 
and the vulva and anus circumscribed by a deep incision. The 
tissues close beneath the pubic arch are now dissected away from 
below and the vulva thrust back beneath the symphysis ; it is now 
seized above the bone, and together with the anus dissected away 
and removed with the other organs. 

The Bladdei^ is first opened and examined. The vulva may now 
be examined for hypertrophies, inflammatory lesions, ulcers, cica- 
trices, cysts, and tumors. The vagina is opened along the anterior 
surface ; its more common lesions are inflammations, fistulae, ulcers, 
tumors, and rarely cysts. 

The Uterus. — Before opening this organ its size and shape 
should be determined. The adult virgin uterus is a pear-shaped 
body, flattened antero-posteriorly ; the upper portion, or body, is 
directed upward and forward, whilst the lower portion, the cerAix, is 
directed downward and baclrvvard. It is covered anteriorly by peri- 
toneum to a point a little below the level of the os internum ; pos- 
teriorly, to a point a little below the level of its junction with the 
vagina. The peritoneal investment separates from the organ at the 
sides to form the broad ligaments. The uterus is held in position 
by the broad and round ligaments and by its attachments to the 
bladder and rectum and vagina. The upper end, the fundus, does 



o 



36 THE METHOD OF MAKING 



tj 



not extend above the level of the brim of the peh'is. Its average 
length is about 7.6 cm. (3 in.) ; its breadth about 5.1 cm. (2 in.) ; its 
thickness about 2.5 cm. (1 in.) ; its average weight is about 31 to 16 
gm. (1 to 1-T oz.). During menstruation the uterus is slightly 
enlarged and the mucous membrane of the body becomes thicker, 
softer, and its vessels engorged with blood ; while its inner surface is 
more or less thickly covered with blood and cell detritus. A descrip- 
tion of the complicated changes in the itterus which pregnancy entails 
nia}' be foimd in the works on obstetrics. After pregnancy the 
uterus does not return to its original size, but remains somewhat 
larger ; the os is wider and frequenth' fissured. 

We not infrequently find in the mucous membrane of the lower 
part of the cervix small transparent, spheroidal structures, called 
ovula Xabothi ; these are small retention cysts caused by the closure 
of the orifices of the mucous glands of the part. The more common 
lesions observed in the uterus are malpositions, malformations, 
lacerations, ulcerations of the cervix, acute and chronic inflammation 
of the mucous membrane or muscularis, or both, thrombosis and 
inflammation of the veins, and tumors. 

In the infant the uterus is small, the body flattened, the cer^dx 
disproportionately large. Duiing childhood the organ increases in 
size, but the body remains small in proportion to the cervix. At 
puberty the shape changes and the body becomes larger. 

The Ovaries are flattened, ovoidal bodies, situated one on each 
side and lying nearly horizontally at the back of the broad ligament 
of the uterus. Their size is variable and they are usually largest in 
the virgin state. Their average weight is from 3.9 to 6.5 gm. (3 to 
5 3). They measure about 3.8 cm. (14- in.) in length, 1.9 cm. 
(f in.) in breadth, and nearly 1.3 cm. (-j in.) in thickness. The sides 
of the ovary and its posterior border are free ; it is attached along 
the anterior border ; to its end is attached the ovarian ligament : to 
its outer extremity one of the fimbriae of the Fallopian tube. The 
ovary is covered on its free surface by cylindrical epithelium, and its 
surface is less glistening than the general peritoneum. The surface 
of the ovary is smooth in the young, but becomes rougher and 
depressed in spots as the process of ovulation goes on. In adult 
females we usually find corpora lutea in their various stages. We 
should seek for e^^dences of acute and chronic inflammations, for 
tumors and cvsts. 

The Fallopian Tubes, lying in the upper margin of the broad 
ligaments, are from 7.6 to 10 cm. (3 to 1 in.) in length. The leng*th 
often differs considerably on the two sides. They commence at the 
upper angles of the uterus as small perforated cords, which become 
larger further outward and bend backward and do^^mward toward 



POST-MORTEM EXAMINATIONS. 37 

the ovary. They terminate in an expanded fimbriated extremity 
about 2.5 cm. (1 in.) beyond the ovary. They are covered by peri- 
toneum, and the mucous membrane Hning them, continuous with 
that of the uterus, is thrown into longitudinal folds. Malpositions 
by adhesions, closure, inflammations, and cysts are the more com- 
mon lesions. The possibility of tubal pregnancy should be borne in 
mind. 

Preservation. — All of these organs and their tumors may be hardened in Miiller's 
fluid. The vagina should be stretched flat on cork and the cavity of the uterus laid 
wide open. Great care should be taken not to touch either the internal surface of 
the uterus or the external surfaces of the ovaries, since in both the epithelium is very 
easily rubbed off. 

It is better, after opening them by a transverse incision, to suspend the ovaries by 
a thread in a jar of the preservative fluid than to let them lie on the bottom, since the 
epithelium is thus less liable to be rubbed off. Larger cysts of the ovary for exhibi- 
tion purposes should be distended with preservative fluid (see p. 53). 

AUTOPSIES IN CASES OF SUSPECTED POISONING. 

It is always best, in cases of suspected poisoning, to preserve for 
the chemist not only the stomach and intestine, but the entire liver 
and brain ; or, if portions of these only can be saved, these portions 
should be carefully weighed, as well as the entire organs, and the 
relative amount of tissue reserved carefully noted at the time. It is 
even well, particularly in cases in which the administration of the 
readily diffusible poisons, such as arsenic, strychnia, etc. , is suspected, 
to preserve the whole of all of the internal organs, together with a 
large piece of muscle and bone; since with large quantities of tissue 
the results of the chemical analysis depend less upon calculations, 
and are hence more comprehensible to the average jury. In all such 
cases jars should, if possible, be procured which have never been 
used before, and these should be carefully washed and rinsed with 
distilled water. They should have glass stoppers and be sealed at 
once and carefully labelled before leaving the hands of the operator. 
If they can be delivered to the chemist without much delav, thev 
should have no preservative fluid added. If they are to be kept for 
a considerable time, pending the action of a coroner's jury or for 
some other reason, a small quantity of pure, strong alcohol may be 
poured over them. In this case the operator should be particular to 
preserve a quantity, at least half a pint, of the specimen of alcohol 
used, in a clean, sealed, and labelled bottle, so that this may be tested 
by the chemist and be proven to be free from the poison. It is better 
in all cases, however, to avoid, if possible, the use of alcohol. In all 
autopsies which may have medico-legal importance full notes should 
be taken by an assistant as the operation proceeds, carefully read 
over immediately afterward, and dated and kept by the operator for 



38 THE METHOD OF MAKLN'G 



future reference. The labelling and disposition of the jars should be 
recorded in the notes. The specimens should not for a moment be 
out of the sight of the operator until they are placed under lock and 
key and seal, or are delivered to some authorized person, so that there 
may be no question of their identity should the case come into court. 



EXA3IIXATI0X OF THE BODIES OF XEAV- 

BORX CHILDREN. 

In examining the bodies of new-born children we may have to 
determine, besides the ordinary lesions of chsease, the age of the 
child, whether it was bom alive, how long it has been dead, what 
was the cause of death. 

GEXERAL IXSPECTION. 

Tlie Size and Age. — Caspar" gives the following description of 
the foetus during the different months of intra-uterine life : 

At the fourth iceeJ-: the embryo is S to 13 mm. (yV to fg- iii-) long. 
The cleft of the mouth and two points indicating the eyes can be 
recognized in the head. The extremities are represented by little 
wart -like projections. The heart can be distinguished ; the liver is 
disproportionately large. The umbilical vessels are not yet formed. 
The entire oviun has about the size of a walnut. 

At the eighth week the embryo is 2.3 to 4 cm. fyV to IfV i^i-) long. 
The head forms more than a third of the entire body ; the mouth is 
very large : the nose and lips can be distingiiished. but not the ex- 
ternal ear. The hand is lono'er than the forearm : the fins^ers are 
formed, but joined together : the toes look hke httle buds : the soles 
of the feet are turned inward. The position of the anus is indicated 
by a point. The abdomen is closed. All the viscera can be recog- 
nized. Centres of ossification are formed in the apophysis of the first 
cervical vertebra, the humerus, radius, scapula, ribs, and cranial 
bones. There are rudimentary external genitals, but the sex can 
hardlv be distinoiiished. The ovum has about the size of a hen's 



AO'O' 



At the twelfth week the placenta is formed. The embryo is 5 to 
6.5 cm. {'2 to 2i in.) long and weighs about 31 gm. The head is 
separated from the thorax by a distinct neck. The eyes and mouth 
are closed. The nails can be perceiA'ed on the fingers. The sex can 
be recognized. The umbihcal cord is inserted near the pubes : the 

1 Caspar, "Handbook of Forensic Medicine." Revised German Edition by Liman, 
or Sydenham Society Translation. 



POST-MORTEM EXAMINATIONS. 39 

muscles begin to be recognizable. The thymus and suprarenal cap- 
sules are formed. The cerebrum, cerebellum, medulla, and the cav- 
ities of the heart can be recognized. The humerus is 1.7 mm. long ; 
the radius 5.5 mm.; the ulna 6.6 mm.; the femur and tibia 4.4 to 
0.6 mm. ; the fibula 5.5 mm. The ovum is as large as a goose's egg- 

At the sixteenth week the embryo is 13 to 15 cm. (5 to 6 in.) long 
and weighs 77 to 93 gm. (2^ to 3 oz). The skin is of a rose-red color 
and has considerable consistence. The formation of fat in the 
subcutaneous tissue has begun. The scrotum and labia are formed. 
The face begins to assume its characteristic appearance. There is 
whitish meconium in the duodenum. The liver is not so dispropor- 
tionately large, and the gall bladder is formed ; the anus is open. 
The length of the humerus, radius, and ulna is 1.7 cm. ; the femur 
and tibia 8.8 to 11 cm. The calcaneus begins to ossify at the middle 
of the fourth month. 

At the tiveutieth tveek the embryo is 26 to 28 cm. (10 to 11 in.) 
long ; it weighs from 225 to 320 gm. (7yV to 10 oz.). The nails are 
quite perceptible. There is a thin down on the head. The head 
is still disproportionately large, occupying about one-fourth of the 
body. There is as yet none of the vernix caseosa. The secretion of 
bile has commenced and stains the meconium. The insertion of the 
umbilical cord is still further off from the pubes. The liver, heart, and 
kidneys are large in proportion to the other organs. The convolu- 
tions of the brain cannot be recognized. The humerus is 2.8 to 3 
cm. long ; the radius 2.6 cm.; the ulna 2.8 cm.; the femur, tibia, 
and fibula, each 2.6 cm. The astragalus and the upper part of the 
sternum begin to ossify. 

From this time on the length of the foetus forms an approxi- 
mately accurate basis for the estimation of its age. From tli is pe- 
riod till its maturity the length of the foetus, deter mined in 
centimetres, corresponds to about one-fifth of the number of 
months of its age. From this time on the weight exhibits marked 
individual differences, and is therefore a less reliable criterion of its 
age than is the length. 

At the tiventy -fourth tveek the embryo is 31 to 34 cm. (12 to 13 
in.) long and weighs 750 to 875 gm. (24 to 28 oz.). The lanugo and 
vernix caseosa are formed. The skin is of a dusky cinnabar-red 
color. The meconium is darker. The scrotum is empty, small, and 
red ; the labia majora are prominent and held apart by the project- 
ing clitoris. The pupillary membrane is present and readily recog- 
nized. The length of the humerus and radius is 3.5 cm. ; of the ulna, 
femur, tibia, and fibula, each 3.7 cm. 

Xt the twenty -eighth week the embryo is 36.4 to 3;> cm. (14| to hH 
in.) long and weighs 1,500 to 1,750 gm. (48 to 57 oz.). The hair is 



40 THE METHOD OF MAKING 

more abundant and longer. The great f ontanelle measures about 4 
cm. (1|- in.) in diameter, and all of the fontanelles are readily per- 
ceived. The skin is of a dirty-reddish color and abundantly beset 
with the lanugo and vernix caseosa. The large intestine contains 
much meconium. The humerus is 4.5 to 5 cm. long; the radius 3.7 
cm. ; the ulna 4 cm. ; the femur, tibia, and fibula, each 4. 2 to 4. 6 
cm. 

At the thirty-second week the embryo is 39 to 41.5 cm. (loi to 
16i in.) long and weighs 1,500 to 2,500 gm. (48 to 81 oz.). The skin 
is lighter in color ; the pupillary membrane has disappeared. The 
testicles are in the scrotum or the inguinal canal ; the labia are still 
w^idely apart and the clitoris prominent. The nails reach nearly to 
the ends of the fingers. The humerus is 5 to 5.2 cm. long; the ra- 
dius 4 to 4.2 cm. ; the ulna 4.8 to 5 cm. ; the femur 5.2 cm. ; the tibia 
and fibula, each 4. 8 to 5 cm. The last sacral vertebra begins to os- 
sify. 

At the thirty -sixth tveek the embryo is 44.2 to 46 cm. (17.4 to 18 
in.) long and weighs about 3,000 gm. (97 oz.). The scrotum begins 
to become wrinkled and the labia to close. The hair becomes more 
abundant, while the lanugo begins to diminish in amount. 

At the fortieth week the foetus is fully developed and the term 
of its intra-uterine life accomplished. 

The fresh corpse of a new-born child at term no longer resembles 
that of the immature foetus. The skin is firm and pale, like that of 
an adult. The lanugo has disappeared except on the shoulders. In 
the majority of cases the hair on the head is 1.5 to 2 cm. (| to | in.) 
long. The great fontanelle is, in the average, 2 to 3 cm. {-^-^ to lyV 
in.) long. As determined by an anabasis of 661 cases, the average 
length is 50 cm. (20 in.), the Aveight 3,256 gm. (105 oz.). The nails 
are hard and reach to the tips of the fingers, but not to those of the 
toes. The cartilages of the ears and nose are hard. The labia are 
more nearly closed. An ossification centre in the lower epiphysis of 
the femur should be sought for, as its presence is one of the most 
reliable signs of the maturity of the foetus. If it is absent the foetus 
is, as a rule, not more than thirty-seven weeks old ; but in rare cases 
it may be absent at term. A centre of ossification 1 mm. (.039 in.) 
in diameter indicates an age of 37 to 38 Aveeks, if the child was born 
dead or died soon after birth. Rarely it is no larger than this at 
term. A diameter, at birth, of 1.5 to 9 mm. (.058 to .351 in.) indi- 
cates an age of 40 weeks. A diameter of less than 9 mm. (.351 in.) 
indicates, as a rule, that the child has lived some time after its birth; 
a less diameter than 7 mm. (.273 in.), however, does not prove the 
contrary. 

Twenty-four hours after the birth of the child the skin is firmer 



POST-MORTEM EXAMINATIONS. 41 

and paler. The umbilical cord is somewhat shrivelled, although still 
soft and bluish in color. From the second to the third day the skin 
has a yellowish tinge and the cuticle sometimes appears cracked. 
The umbihcal cord is brown and dry. From the third to the fourth 
day the skin is yellower, and the cuticle is apt to separate from the 
skm. The umbilical cord is of a brownish-red color, flattened, semi- 
transparent, and twisted. The skin around its insertion is red and 
congested. 

The head should be examined for the marks of injuries Very 
commonly some portion of the scalp will be found swollen and mfil- 
trated with blood and serum. This may be the caput succedaneum 
formed during delivery. The mouth and nose should be examined 
for the presence of any foreign bodies which might have caused suf- 
focation. 

The neck should be examined for marks of strangulation The 
umbihcal cord may be twisted around the child's neck and strangle 
It. The mark left by the cord is usually continuous, broad, not ex- 
coriated, sometimes accompanied by ecchymoses in the skin 

The entire body should be examined for the presence of vernix 
caseosa, blood, marks of injury, and the existence of putrefaction 
It should be remembered that putrefaction is apt to commence ear- 
her m the bodies of young children than in those of adults 
.1. ^Jl^^'l''^^^'^^^ ^^^^ may be cut or torn. It usually separates br 
the fifth day, sometimes not until the tenth. If the umbilicus is cica- 
trized and healed the child has probably lived for three weeks 1 
zone of redness around the insertion of the cord may exist previous 
to birth. Eedness and swelling (which may disappear after death) 
with suppuration can only be found in a child which has lived for 
several days. The drying and mummification of the cord mav take 
place as well m dead as in living children. It is possible for a child 
to die by haemorrhage from a cut or torn cord, either before or after 
it lias breathed. 

The extremities may exhibit fracture of the bones. These mav 
occur durmg intra-uterine life, from injuries to the won.an or from 
unknown causes ; or may be produced by violence in delivery or bv 
injuries after birth. ^ ' 

INTERNAL EXAMINATION. 

The Head.-The f ontanelles and sutures should first be examined 
as to their size and for penetrating wounds. An incision should then 
be made throiig-h the scalp across the vertex, and the flaps turned 
backward and forward as in the adult. With a small knife the 
edges of the bones should be separated from the membranous sutures 
and the dura mater, beginning low down in the frontal and 



going 



42 THE METHOD OF MAKING 

back into the lambdoidal suture on either side. The bones are then 
drawn outward and cut through around the skull -^dth strong scis- 
sors. The brain is removed and examined as in the adult.' 

Effusions of blood — cephalhaematoma — may be formed, soon after 
birth, between the pericranium and bone, or, more rarely, betvveen 
the dura mater and bone. Clots are also f oimd between the dura 
mater and skuU : between the dura and pia mater ; more rarely in 
the substance of the brain, as the result of protracted or instrumental 
dehveries, or of injuries after birth. 

The cranial bones may be maKormed, or exhibit the lesions of 
rickets or caries, or be indented, fissured, or fractured. These latter 
lesions may be produced duiing intra-uterine hfe by injuries to the 
mother, by unknown causes, by difficult dehveries, or by direct ^-io- 
lence after birth. 

In cases of chronic internal hydrocephalus in young childi^en, in 
which the ventricles are much dilated and the brain substance thinned 
over the vertex, the brain is very apt to be torn in removal, and the 
amoimt of dilatation thus becomes difficult of determination. It is, 
therefore, better in such cases to place a pail of water beneath the 
head, or even immerse the latter in it, and remove the brain in the 
water. In this way it floats after removal, supported on all sides. It 
may now be opened in the water and the extent of the lesion deter- 
mined at once, and parts saved for microscopical examination. 

If it be desu-ed to preserve the brain for demonstration of the le- 
sion or for a museum specimen, it should be transferred unopened to a 
large jar containing a mixtiu-e of equal parts of alcohol and water. A 
portion of the ventricular fluid should now be removed with a syringe 
provided ^vith a small canula, and replaced by strong alcohol. This 
may be done by puncturing the ventricles from below. The fluid in 
the jar, as weU as in the ventricles, should be changed in forty-eight 
hours and then graduaUy increased in strength until the organ be- 
comes hard. The brain mav then be cut transverselv across, when 
the degree of dilatation of the ventricles, etc., will be revealed. The 
brain, of course, shrinks considerably by this process, but the rela- 
tive proportions are approximately preserved. 

The brain is normally much softer and pinker than in the adult, 
the pia more dehcate : both may be much congested or anaemic ■v\'ith- 
out known cause. The ventricles contain very httle seriun. MaKor- 
mations, apoplexies, hydrocephalus, simple and tubercular inflamma- 
tory lesions, are to be looked for. 

Spinal Cord, — Extravasations of blood between the membranes 
of the cord may occiu* from the same causes as those in the brain. 
Spina bifida is the most frequent malformation. 

^ Or an incision througti the bones with, a fine saw may be made as in the adult. 



POST-MORTEM EXAMINATIONS. 43 

The Thorax and Abdomen. — These are opened as in the adult. 
The peritoneal cavity contains a very httle clear serum. A red 
fluid may be produced by decomposition. The peritoneum is often 
the seat of intra-uterine inflammation. 

The Diaphragm. — In still-born infants its convexity reaches to 
the fourth or fifth rib. After respiration it reaches a point between 
the fourth and seventh ribs. Its position is, however, so variable 
that it is of little diagnostic importance. 

The Thorax. — The thymus gland, at this period very large, occu- 
pies the upper portion of the anterior mediastinum, covering the tra- 
chea and large vessels. Its average weight is about 15.5 gm. (i oz.). 
It is usually about 5 cm. (2 in.) long, 3.8 cm. (l^ in.) wide at its 
lower part, and about .63 to .85 cm. (J to ^ in.) in thickness. It may 
be hypertrophied and compress the large vessels, or be inflamed and 
suppurating. 

The heart lies more nearly in the median line than in the adult. It 
weighs from 46 to 108 gm. (1^ to 3i oz.). The ventricular walls are 
of nearly equal thickness. The pericardium contains very little se- 
rum. A considerable quantity of red fluid may accumulate here as a 
result of decomposition. There may be small extravasations of blood 
beneath the pericardium in still-born children and in those born alive. 
Pericarditis with effusion of serum and fibrin, and endocarditis with 
consequent changes in the valves, may exist before birth. Malfor- 
mations and malpositions of the heart cavities and large vessels are 
not infrequent. The time of closure of the foramen ovale and the 
ductus arteriosus varies very widely in different cases. 

The pleural cavities contain very little serum, but decomposition 
may lead to the accumulation of a considerable quantity of red fluid. 
Small extravasations of blood in the subpleural tissue may be found 
in children which have died before birth and after protracted labors. 
Inflammation, with exudation of serum, fibrin, and pus, may exist 
before birth. 

The lungs in a still-born child are small, do not cover the heart, are 
situated in the upper and posterior portion of the thorax, are of a dark- 
red color and of firm, liver-like consistence, and do not crepitate. In 
a child born alive, and which has respired freely, the lungs fill the 
thoracic cavity, but do not cover the heart as much as in the adult ; 
they are of a light-red or pink color, and crepitate on pressure. If re- 
spiration has been incompletely performed we find various intermedi- 
ate conditions between the foetal and inflated states. 

If any doubt exists as to respiration having taken place, it is cus- 
tomary to employ the hydrostatic test. This is done by placing the 
lungs, first together, then separateh^ and afterward cut into small 
pieces, in water. It is commonly said that if they sink the child has 



44 THE METHOD OF MAKING 

not breathed ; if they float it has. This test is not, however, a certain 
one. Taylor says regarding it : 

1. That the hydrostatic test can only show whether a child has or 
has not breathed, not whether it was born alive or dead. 

2. That the lungs of children who have lived after birth may sink 
in water, owing to their not having received air or to their being in 
a diseased condition. 

3. Tliat a child may live for some time with the lungs only partly 
inflated. 

4. That a child may live for twenty-four hours when no part of its 
lungs has been penetrated by air. 

5. The sinking of the lungs is no proof that a child has been born 
dead. 

6. That the lungs of children which have not breathed and have 
been born dead, may float in water from putrefaction or artificial in- 
flation. 

The lesions of inflammation, and vesicular and subpleural emphy- 
sema, may be found in the lungs of new-born children. 

The pharynx should be opened and examined for foreign bodies. 

The larynx and trachea should be examined for the lesions of in- 
flammation and for injuries to the cartilages. 

The thyroid gland weighs about 12 gm. (3 3 ). It may be so 
enlarged as to interfere with respiration. 

The Abdomen. — The kidneys are lobulated and proportionately 
larger than in the adult. There may be ecchymoses on their surface ; 
inflammation ; deposits of uric acid and urates in the tubules of the 
pyramids ; cystic dilatation of the tubules, sometimes reaching an 
enormous size. There may be absence or retarded development of 
one kidney. Malformations and malpositions of the kidneys are of 
frequent occurrence. 

The suprarenal capsules are large. They may be dilated into 
large cj^sts filled with blood. 

The spleen is large and firm. It may be abnormally enlarged, 
and its surface is soraetimes covered with fresh inflammatory exuda- 
tions. 

The intestines. In the small intestines inflammation and swell- 
ing and pigmentation of the solitary and agminated f olhcles (lymph 
nodules) are sometimes found. The large intestine usually contains 
meconium, but this may be evacuated before or during birth. The 
sigmoid flexure is not as marked as in the adult. 

The formation of gas in the stomach and intestines does not usually 
take place until respiration is established. If decomposition has com- 
menced, however, gas may be formed as a part of the process. 

The liver is of a dark-red color, is large, and contains much blood. 



POST-MORTEM EXAMINATIONS. 45 

Its size diminishes after respiration is established. The size is so vari- 
able, before and after respiration, that it gives little information as to 
the age of the child. Large extravasations of blood are sometimes 
found beneath the capsule of the liver without known cause. A 
variety of pathological conditions, fatty and waxy degeneration, 
gummy tumors, etc. , may be found. 

The bladder may be full or empty, both in still-born children and 
in those which have breathed. Dilatation and hypertrophy may exist 
during intra-uterine life. 

Generative Organs. — The external generative organs in both 
males and females are more prominent than in adults. The ovaries 
are high up in the pelvis and large ; the cervix uteri is long ; the body 
small and lax, resting forward against the bladder. Phimosis in the 
male is the normal condition. Malpositions and retarded develop- 
ment of the testicles should be noticed. It should be observed 
whether the anus is perforate. 

The Bones, in suspected cases, should be examined for the 
lesions of inflammation, rickets, and syphilis. 

Preservation. — The various foetal tissues may be preserved by the same methods 
as are employed for those of the adult ; but as they are very delicate they should be 
handled with great care and the preservative fluids changed with sufficient frequency. 



GEXEEAL ^lETHODS OF PEESEEYIXG 

PATHOLOGICAL SPECIME]^S AXD PEE- 

PAEIISTG THEM FOE STUDY. 



It is not our purpose in this section to give a complete account of 
the technical procedures required in the study of pathological speci- 
mens, since the methods are for the most part identical "svith those 
employed in the study of normal tissues, with which the student or 
practitioner is presumably famihar before prosecuting pathological 
studies. We "^Wsh simj)ly to give a few brief hints as to the general 
methods which we have found most useful. Additional details ^^411 
be found in parts of the book deahng Avith special tissues and organs. 

The Study of Fresh Tissues. — Although for the most part the 
conditions for the minute study of tissues are more favorable after 
they have been hardened in some preservative agent, it is yet in 
many cases very important to examme them in the iresh condition. 
For this purpose they may be teased apart in a one-half -per-cent 
solution of sodium chlorid and mounted and studied in the same. 
The same solution mav be used for stud^T.no; semi-fluid substances, 
such as exudations from the mucous membranes, pus cells, etc. 
These preparations are not suitable for permanent mounting, as they 
do not keep well. 

For staining the elements of fresh tissues, particularly the nuclei, 
and at the same time hardening them so that they can be mounted 
and preserved for some time, Carnoy's solution is of great value. It 
is made by adding to a saturated aqueous solution of methyl green 
one per cent of acetic acid and one-tenth per cent of osmic acid. The 
tissue is immersed or teased in this solution, and after three to five 
minutes the color washed off and the specunen mounted in salt solu- 
tion or in a mixture of equal parts of salt solution and glycerin. 

Thin sections of fresh tissues may be prepared by the use of some 
of the forms of the freezing microtome. That form de\dsed by Thoma 
and made by Jung, of Heidelberg, is simple, cheap, and effective. 

Frozen sections may be stained in an aqueous solution of safranin 
and then mounted in a mixture of equal parts of glycerin and water. 



GEI^ERAL METHODS OF PRESERVING PATHOLOGICAL SPECIMENS. 47 

Decalcifying. — Bones which are the seat of lesions, or calcified 
tissues, must be freed from lime salts before thin sections can be 
made from them. This may be accomplished by the use of a satu- 
rated aqueous solution of picric acid. The bone or other tissues 
should be cut into small pieces, not larger than a cubic centimetre, 
and suspended by a thread in a large quantity of the fluid, which 
should have an excess of picric acid crystals at the bottom, and 
should be frequently shaken. .Considerable time is required for de- 
calcification by this method. 

If it be necessary to decalcify more rapidly, chromic acid may be 
used at first and the process completed by nitric acid. The small 
pieces of bone are suspended at first in a one-sixth-per-cent aqueous 
solution of chromic acid. After two or three days the strength of 
the solution is increased to one-quarter per cent and after three days 
to one-half per cent. After another week the fluid should be changed 
and one per cent of nitric acid should be added. This fluid should be 
renewed every three days until the decalcification is complete, which 
may be determined by passing a fine needle through the specimen. 
The specimen should now be thoroughly soaked in water to remove 
all traces of the acid, and, after lying for a day or two in strong 
alcohol, is ready for embedding and section cutting. 

Another method of rapid decalcification which gives excellent, and 
perhaps the best, results is by the combination with nitric acid of 
pliloroglucin, the latter agent preventing the swelling of the tissue 
elements. One gramme of phloroglucin is dissolved with gentle 
heat in 5 c.c. of nitric acid. This solution, when effervescence has 
ceased, is of a ruby-red color. To this are added 70 c. c. of strong al- 
cohol and 30 c.c. of water. Small pieces of bone are suspended by 
thread in relatively large quantities of this fluid. In from one to 
twenty-four hours, depending upon the size of the piece of bone, the 
decalcification is usually complete, as may be ascertained by the 
needle test. ]^ow wash the specimens thoroughly in running water 
until no acid reaction is given by litmus paper; put for twenty-four 
hours in eighty-per-cent alcohol, and then in strong alcohol. Bone 
decalcified in this way is apt to stain much better with hematoxylin 
and eosin than after the use of the chromic and nitric fluid or picric 
acid. 

Hardening and Preservation. — In the majority of cases patho- 
logical specimens are best hardened first in Miillers fluid ainXXhe 
process completed by alcohol. Miiller's fluid is made by the follow- 
ing formula : 

Potassium Bichromate '2 parts. 

^* Sulphate 1 part. 

Water 100 parts. 



48 



GENERAL IMETHODS OF PRESERVIXG 



The specimens, which should be cut into small pieces not more than 
1 or 2 cm. square, are placed in a large quantity of the fluid, at least 
ten times the bulk of the specimen, and allowed to remain for two or 
three weeks. The fluid should be changed three or four times within 
the first ten days, and after this as often as it becomes turbid 
or a sedunent forms. After the specimens have acquired consider- 
able consistence, or have been in the fluid for the proper time, they 
are removed from the fluid and soaked for from twenty-four to forty- 
eight hours in water, which should be frequently changed. They 
are then placed in equal parts of alcohol and water for forty-eight 
hours, and then in strong alcohol, by means of which the hardening 
is completed. They may be preserved in eigiity-per-cent alcohol. 

For the special directions for hardening nerve tissues see page 16. 

Alcohol. — If specimens are beginning to decay they should, as a 
rule, be put at once into strong alcohol, which gives the best hope of 
useful material. For routine hardening, when topographical features 
rather than minute textural details are to be studied, alcohol used 
alone is a most useful hardening agent. It may be used in strength 
of fifty or sixty per cent for twenty-four hours, after which the speci- 
mens are put in strong alcohol (ninety to ninety -five per cent). 

Osmic Acid is of great value for the hardening of small portions 
of delicate tissues, since it serves to fix the elements in a nearly nor- 
mal condition and stains them of a brown or black color. It is gene- 
rally used in one-per-cent aqueous solution, the tissues being placed 
in it when quite fresh and allowed to remain for twenty-four hours. 
They are now washed in water and may be preserved in a mixture of 
equal parts of glycerin, alcohol, and water. Such preparations are 
best adapted for teasing or isolation by other methods than section 
cutting. If it is desired to make sections of sohd tissues preserved in 
osmic acid, the latter should be introduced by interstitial injection, 
and the fragment immersed in the acid for twenty-four hours, and 
then removed, washed, and placed in strong alcohol. Instead of 
using the one-per-cent osmic acid pure, very good results are obtained 
by diluting it ^vith an equal volume each of water and strong alco- 
hol. This is in many cases preferable, since the tissues are not 
stained so dark by the acid, and are more readily preserved subse- 
quently in alcohol. 

Flemming's Osmic Acid Mixture. — For the purpose of fix:ing 
dehcate tissue elements to show ixdnute structiu'al detail, such as 
mitotic figures, this mixture is of great value. It is made of — 



One-per-cent solution of Chromic Acid 15 parts. 

Two-per-cent solution of Osmic Acid. . . • -l " 

Glacial Acetic Acid 1 part. 



PATHOLOGICAL SPECIMENS. 49 

This mixture does not keep well and hence should be made up in 
small quantities. Small portions of tissue should soak in the mixture 
for about one-half hour, and then, after thorough washing in water, 
are put for twenty-four hours in seventy-per-cent alcohol, then trans- 
ferred to strong alcohol, in which they are kept. 

DelafielcVs Alcoholic, Osmic Acid Mixture. — This consists of — 

One-per-cent solution of Osmic Acid 10 c.c. 

One-fif th-per-cent solution of Chromic Acid 100 

]N^inety-five-per-cent Alcohol 100 

Acetic Acid 1 



a 
a 
a 



After remaining for twenty-four hours in this solution the specimens 
are transferred to eighty-per-cent alcohol, in which they may be per- 
manently kept. This solution is very efficient in preserving the cells 
of the parenchyma of such organs as the kidney and liver in a nearly 
natural condition. 

Corrosive Sublimate is a most excellent fixative for delicate 
structures. It does not penetrate dense tissues readily, and hence all 
pieces of tissue should, when it is used, be very small. 

For general use Lang's solution is to be recommended. The 
formula is — 

Mercuric Chlorid . 5 gm. 

Sodium " 6 gm. 

Hydric Acetate 5 c.c. 

Water 100 '*' 

The tissue remains in this mixture from half an hour to an hour. 
Specimens fixed in sublimate do not stain well, and become brittle 
unless the excess of sublimate is removed. This can be larsfelv done 
by prolonged washing in running water. But it is much more easily 
and certainly accomplished by the chemical action of dilute iodine 
solution. The specimen is removed from the sublimate mixture and 
put at once into seventy-per-cent alcohol. To this is added from time to 
time a sufficient quantity of saturated alcoholic solution of iodine (or 
tincture of iodine) to give the alcohol a moderately deep iodine color. 
At first this color gradually disappears, and the iodine solution should 
be repeatedly added until the color persists. The specimens are now 
transferred to seventy-per-cent alcohol, and after twentj^-four hours 
to strong alcohol. 

A very excellent preservation of fragments of tissue to show 
minute cell structure, mitotic figures, etc., may be obtained by scrap- 
ing the cut surface of an organ, tumors, etc., and droj^ping the 
scrapod-off mass into the sublimate solution. This, after from i^ne 
to live minutes, is decanted, the tissue fragments thorougldy and 

repeatedly washed in water and finallv preserved in alcoliol. These 

4 



50. GENERAL METHODS OF PRESERVING 

II tiny cell clusters may now be embedded in a mass in celloidin (see 

below), and from this sections of extreme thinness may be obtained. 

Chromic Acid Mixtiu^e. — For many purposes a ver}^ excellent 
hardening may be obtained by using a mixture of one-sixth-per-cent 
aqueous solution of chromic acid 2 parts and alcohol 1 part. This 
fluid, like all others, should be frequently changed, and the harden- 
ing may be finally completed with alcohol. This is commonly spoken 
of simply as the chromic acid mixture. 

Although the above is the routine method of hardening tissues, 
departures from it are occasionally desirable in the preparation of 
different organs or for the accomplishment of special ends. Thus, in 
some cases — as in the kidneys, for example — the preservative fluids 
are brought into more direct and immediate contact with the tissue 
elements if they are injected under low pressure directly into the 
blood vessels. Or by means of a hypodermic syringe the fluids may 
be thrown directly into the interstices of the tissue by thrusting the 
needle into them and slowly injecting the preservative agent. This 
is called interstitial injection. 

Pathological specimens which occur, or are isolated in the form of 
membranes, should be stretched with pins on a piece of wood or flat 
cork before being immersed in the preservative fluids. 

Minute structures, such as occur in exudations from the mucous 
membranes and in cyst fluids, renal casts, etc. , may be preserved by 
allowing them to settle, decanting as much of the fluid as possible, 
and then adding a considerable quantity of Mliller^s fluid, which 
after a few days should be decanted and replaced by water. The 
latter should be renewed by decantation several times, and finally the 
sediment may be preserved in a mixture of equal parts of glycerin, 
water, and saturated aqueous solution of picric acid or alcohol. 

Embedding and Section Cutting. — Some dense tissues, after be- 
ing well hardened, are sufficiently solid to permit of thin sections be- 
ing made from them without further preparation, but in most cases 
very thin sections cannot be prepared without filling the interstices of 
the tissue with some embedding material, which gives it greater con- 
sistence and holds the tissue elements firmly in their natural relations 
to one another while the section is being made. Cacao butter, wax, 
paraffin, and various other substances have been largely used for this 
purpose and are very useful ; but the more recently employed cel- 
loidin is by far the most valuable material, and may be used in 
nearly all cases. 

Celloidin, a non-explosive, purified form of gun-cotton, is best ob- 
tained in the form of thin shavings, since it is most easily dissolved 
in this form. A strong solution is made in equal parts of sulphuric 



PATHOLOGICAL SPECIMENS. ol 

■ether and alcohol. The solution should have the consistence of thick 
molasses. The specimen, having been soaked for twenty-four hours 
in a mixture of equal parts of alcohol and ether, is placed in the cel- 
loidin solution, where it remains until permeated by it. This will or- 
dinarily occur, if the specimen be of moderate size, in from twelve to 
twenty-four hours. For this preliminary soaking the celloidin solution 
may be a little thinner than above mentioned. If the specimen be 
small and require but little support, it may now be laid directly on the 
end of a small bit of wood and a few drops of celloidin poured around 
it. In most cases, however, it is better to make a small paper box, in 
which the specimen is placed in a proper position and the celloidin 
poured in around it so as to completely enclose it. In either case a 
considerable quantity of celloidin should be poured around the speci- 
men, since the celloidin shrinks considerably in hardening. If sec- 
tions are to be cut with the microtome the paper box should be made 
by winding a strip of thin paper around the end of a short cylinder of 
wood,' allowing it to project for a sufficient distance beyond the end. 
The paper is held in place by a rubber band. We have thus a cylin- 
drical box with a wooden bottom projecting below it by which the 
whole can be held in the clamp of the microtome. 

After the specimen, either free on the end of the cork or in its box, 
is surrounded by celloidin, it should be allowed to stand for a short 
time exposed to the air, so that it may harden on the outside by the 
evaporation of the ether. If the temperature be high the too rapid 
evaporation of the ether will cause bubbles to appear in the mass. 
This should be avoided by covering the specimen with a bell-jar. 
After the celloidin mass has acquired sufficient hardness on the out- 
side to keep its shape, the whole should be floated, specimen side 
down, in seventy- or eighty-per-cent alcohol, in which the celloidin will 
harden and acquire a sufficient consistence for cutting in a few hours. 
When this is accomplished the paper may be stripped off, and the 
specimen is ready for section cutting. A little practice ^\^11 teach the 
operator of what consistence to make the celloidin solution, how long- 
to expose to the air, etc. 

After the sections have been cut they may be stained in the usual 
way (see below) and mounted in glycerin or balsam. If mounted in 
balsam, the oil of cloves, which is ordinarily used for clearing up the 
sections, will dissolve the celloidin. For some tissues this does no 
harm, since they are firm enough to hold together even in thin sec- 
tions ; but in handling friable and delicate tissues it is well to keep 
tlie celloidin in place, mounting it with the specimen, ^Wth the study 

' The short wooden cylinders of various sizes, known as "deck plugs," are very 
convenient for this purpose. They are cheap and may be bought of dealers in 
shipbuilders' supplies. 



52 GENERAL METHODS OF PRESERVING 

of which it does not interfere. This may be accomplished by using 
the oil of origanum instead of oil of cloves for clearing. 

The uncut portion of tissue may be preserved, embedded in cel- 
loidin, by keeping it in eighty-per-cent alcohol. 

It is better, in permanent preservation of uncut celloidin-embedded 
specimens in bulk, to cut them off from the wooden block, since the 
prolonged action of the alcohol on this often gives rise to a dark ma- 
terial which colors the specimen and interferes with the staining of 
sections made later. The severed specimen can be readilyre fastened 
to a fresh bit of wood by a drop of celloidin when more sections are 
to be made. 

Section Cutting may be done by the free hand with a razor 
gromid flat on the lower side, but better sections can be obtained by 
means of a microtome. One of the most useful of these is Thoma's, 
which is made in three sizes, the intermediate or the larger one being 
the more useful. The Schanze microtome is also well adapted for 
general work, as are some of the American instruments made on the 
same plan. 

Methods of Staining. — Sections of hardened tissues may be 
stained for microscopical study in a variety of ways, but for routine 
work the double staining with hsematoxylin and eosin is most gene- 
rally useful and applicable to nearly all cases. 

The solution of hsematoxylin is prepared as follows : To make 600 
c.c. of the solution take 400 c.c. saturated solution of ammonia alum, 
and add to this -4 gm. crystallized hsematoxylin (Merck's) dissolved 
in "25 c.c. strong alcohol. This is exposed to the light in an unstop- 
pered bottle for three or four days, when the color will gradually 
change from a dirty-red to a deep bluish-purple color. The solution 
is now filtered and 100 c.c. each of glycerin and Hasting's wood 
naphtha are added. After standing for a day or two the solution is 
filtered, allowed to stand for another day, and again filtered ; and 
this is repeated until a sediment no longer forms in the fluid. 

The solution is now ready for staining, and should be consider- 
ably diluted with water as it is used, the best results being obtained 
by diluting the fluid with from ten to twenty times its bulk of wa- 
ter. The sections are immersed in the fluid, and allowed to remain 
until they have acquired a distinct purple color which persists after 
rinsing in water. They are now placed for a moment in a dilute al- 
coholic solution of eosin, and then mounted in glycerin which has 
been colored lightly with an alcoholic solution of eosin. In this way 
the nuclei of the cells will be stained of a purple color, while the 
cell bodies, and to a certain extent the intercellular substance, vdW 
be colored a light rose-red. 

If specimens are to be mounted in Canada balsam, they are stained 



PATHOLOGICAL. SPECIMENS. 53 

Tnth hgeinatoxylin as before, and the eosin staining is done by ting- 
ing with eosin the alcohol with which the final dehydration of the 
specimen is accomplished. 

Methods of Preserving Specimens for Gross Demonstration 
and for Museums. — When specimens of diseased tissues or organs 
are to be preserved entire for exhibition in jars in a museum, it is 
in most cases desirable first to get rid of the blood. This may be 
accomplished, as a rule, by putting them for twenty-four hours in 
running water, after they have been sufficiently opened so that the 
water can get to them. They are now brought into proper condition 
by the removal of superfluous parts and the requisite dissections. 
Then they are carefully brought into the position and form which it 
is wished to preserve by stuffing with horsehair or absorbent cotton 
and by the use of thread. When thus carefully adjusted they are 
either suspended or laid on a wad of absorbent cotton in sixty- to 
eighty-per-cent alcohol. In this they usually become hard, and are 
finally, after the removal of the temporary stuffing and braces, trans- 
ferred for permanent exhibition to fresh, clear eighty-per-cent alcohol. 
This description applies especially to such specimens as have cavities 
to distend or display. 

The more simple specimens, such as the solid viscera, tumors, etc. , 
may be freed from blood in the same way and hardened in sixty-per- 
cent alcohol. 

Firm- walled cysts of various kinds are well preserved in a natural 
condition of distention by drawing off the natural contents through 
a fine canula and refilling with and immersing in the following solu- 
tion, known as Flemming's Chromic and Acetic Acid Mixture : 

One-per-cent Chromic Acid solution ... 20 parts. 

" " Acetic Acid solution 10 " 

Water 70 '' 

After soaking for forty-eight hours in this mixture the tissue, as 
far as it has penetrated, becomes firm and stiff and of a greenish- 
gray color. The specimen is now washed thoroughly in running- 
water and preserved in eighty-per-cent alcohol. 

Cysts, such as echinococcus cysts, small embryos in their mem- 
branes, cystic kidneys, etc., may be preserved in a nearly natural 
condition by placing them in a five-per-cent aqueous solution of 
chloral hydrate, and after a week replacing this by a ten-per-cent 
solution of the same, in which they may be permanently preserved. 
Such specimens are almost equally well preserved in a saturated 
aqueous solution of chloroform. 

Specimens which it is desirable to keep fen- a few days in a natural 



54 GENERAL METHODS OF PRESERVING PATHOLOGICAL SPECIMENS. 

condition for the purpose of demonstration may be placed in the f ol- 
loA^^ng sohition : 



i Water 1,000 c.c. 

r 
J' 
J - 



Common Salt 100 gm. 

Saltpetre. 25 " 

Carbolic Acid 5 " 

Glycerin 15 '* 

Amylic Alcohol 50 " 

(Or Ethylic Alcohol 100 ") 

This fluid is especially well adapted to the preservation of mucous 
membranes, such as that of the intestines, in a nearly natural condi- 
tion for a few days. The specimens should be set in a cool place. 

We would most urgently commend to the reader the impor- 
tance of putting pathological specimens which are to be hardened and 
subsequently examined microscopically, at the earliest possible mo- 
ment into the preservative fluids, which should always be abundant. 
And, furthermore, when specimens are large it is very desirable to 
cut them open, so that the fluids may come into direct contact with 
the tissues. It should be borne in mind that immediately after death 
or the removal of parts from the body, especially in warm weather, 
changes commence in the tissues and progress very rapidly, so that 
in some cases a few hours" or even a few moments' delay will not 
only render subsequent microscopical examinations difficult and 
unsatisfactory, but may lead to serious errors. As above stated, 
Muller's fluid and alcohol are the most generally useful agents. 
Carbolic acid and glycerin should not he used, even for the tem- 
porary preservation of fresh tissue. They not only do not harden 
and preserve the tissue elements, but they — especially glycerin — render 
them almost AvhoUy useless for microscopical examination. 

The not uncommon practice of wrapping a specimen in a cloth 
soaked in alcohol or carbolic acid, and permitting it to remain in this 
for hours or days, is of no use whatever in preserving specimens 
of which microscopical examinations are to be made. Almost 
equally useless is the too common practice of placing a specimen in 
a bottle which it nearly fills, and pouring a little preservative fluid 
around it. ^ot only should the proper fluid be used, but it should 
be abundant, and the specimen so prepared and arranged that it may 
come into direct contact with it. 



PART II. 

OHAISTGES IE THE CIEOULATIOJSr OF THE 

BLOOD. 

CHAH"GES liSr THE COMPOSITIO]^ AND 
STRUCTURE OF THE BLOOD. 

HYPERTROPHY, REGEXERATIO::sr, 
DEGEISTERATIOiSr, ETC. 

II^FLAMMATIOK 

ANIMAL AND VEGETABLE PARASITES. 

INFECTIOUS DISEASES. 

TUMORS. 



OHAjNTGES IK" THE CIRCULATION OF THE 

BLOOD. 



HYPER.^MIA AND ANEMIA. 

There is an inijDortant series of changes in the character of the 
circulation during life which may, when death ensues, either alter 
considerably in appearance or disappear altogether. Among the 
more important of these changes are hypercemia — excess of blood in 
a part ; and ancemia — deficiency of blood in a part. These condi- 
tions and the causes which lead to them will not be described in de- 
tail in this book, which has chiefly to do with alterations of the tissue 
which persist and may be studied after death. Tissues which have 
been the seat of a temporary, and sometimes of a prolonged, hyperce- 
mia, may show to the naked eye nothing abnormal after death, or 
they may look redder than normal ; they may be oedematous, and 
more blood than usual may flow from them when incised. On micro- 
scopical examination the blood vessels may be normal in appearance, 
or more or less distended with blood. Long-continued hypercemia 
may lead to haemorrhage and transudation, to pigmentation, to 
hyperplasia of tissue, or to an atrophy of tissue through pressure, c)r 
even to death of tissue. 

The paleness which is characteristic of anceniic tissues may not 
be evident after death. Anaemia may lead to no recognizable micro- 
scopical changes. On the other hand, if long continued it may in- 
duce atrophy and fatt}' degeneration, and, if excessive, may lead to 
death of tissue. 

HEMORRHAGE AND TRANSUDATION. 

Hceniorrhage is an escape of blood from the heart or vessels. It 
may occur from a rupture of the walls of the vessels, and is then 
called haemorrhage by I'Jie.vis. The rupture may be occasioned by 
injury, by some disease of the walls of the vessels which renders them 
too weak to resist the blood pressure from within, or it may occur 
from the blood pressure in the thin and incompletely devoloiK\l walls 
of new-formed vessels in irranulation tissue, tumors, etc. 



58 CHANGES IX THE 

Under other conditions, without recognizable changes in the walls 
of the vessels, all the elements of the blood may become extra vasated 
by passing, without rupture, through the walls of the vessels. This is 
called haemorrhage by diapedesis. These haemorrhages are usually 
small, but may be very extensive. They usually occur in the smaller 
veins and capillaries, the cells and fluids of the blood passing out 
through the cement substance between the endothelial cells. Al- 
though no marked morphological changes have as yet been detected 
which explain this extravasation, it is probable that some change in 
the nutrition of the walls does occur which renders them more perme- 
able. Haemorrhage by diapedesis is apt to occur as a result of venous 
congestion, or when the flow of blood in the smaller vessels has been 
suspended for some time ; or it may result from the action of some 
poison, or from an injury not leading to rupture ; or it may occur in 
incompletely developed blood vessels, in tumors and other new-formed 
tissues. 

In the extravasation of blood by diapedesis the white blood cells 
may pass through the walls of the vessels, partly at least in virtue of 
their amoeboid movements ; the red ceils, on the other hand, having'^ 
no power of spontaneous movement, are, according to Arnold, car- 
ried passively through the walls by minute currents of fluid which, 
under the changed condition, stream in increased force and volume 
through the endothelial cement substance into the lymph spaces 
outside. 

The altered condition of the blood vessels leading to haemorrhage 
may be local or general, and in the latter case it may either be con- 
genital, as in some cases of the haemorrhagic diathesis, or it may be 
the result of some general disease, as scurvy, purpura, etc. The 
presence of bacteria in the vessels, as in malignant endocarditis and 
in haemophilia neonatorum, is believed in some cases to produce 
changes in the walls of the vessels, leading to extravasation. 

Very small haemorrhages are called petechice ; larger, diffuse ac- 
cumulations of blood in the interstices of the tissues are commonly 
called ecchymoses or sugg illations. A complete infiltration of a cir- 
cumscribed portion of tissue with blood is called a hcemorrhagic in- 
farction. A collection of blood in a tumor-like mass is called a 
hcematoma. Sometimes the elements of the tissue into which the 
blood escapes are simply crowded apart ; sometimes, as in the brain, 
they are broken down. 

The extravasated blood in the tissues usually soon coagulates, 
although exceptionally it remains fluid for a long time. A certain 
number of the white blood cells may wander into adjacent lymph ves- 
sels, or they may remain entangled with the red cells in the meshes 
of the fibrin. The fluid is usually soon absorbed ; the fibrin and a 



CIRCULATION OF THE BLOOD. 51> 

portion of the white blood cells disintegrate and are absorbed. Tlie 
red blood cells soon give up their haemoglobin, which decomposes and 
may be carried away or be deposited either in cells or in the intercel- 
lular substance at or near the seat of the hemorrhage, either in the 
form of yellow or brown granules or as crystals of hsematoidin. 
Sometimes all trace of extravasations of blood in the tissues disap- 
pears, but frequently their seat is indicated for a long time by a 
greater or less amount of pigrnent or by new- formed connective tis- 
sue. Occasionally the blood mass, in a more or less degenerated con- 
dition, becomes encapsulated by connective tissue, forming a cyst. 

Ty^ansudation is the passage, through the walls of the blood ves- 
sels into the lymph spaces outside, of fluid from the blood, with little 
or no admixture of its cellular elements. This occurs constantly, to 
a certain extent, under normal conditions, and forms the commence- 
ment of the lymph circulation. But when the amount of fluid pass- 
ing through the walls of the blood vessels is increased, or its outflow 
into the larger lymph trunks is hindered so that it accumulates in un- 
due quantity in the interstices and lymph channels of the tissues, the 
condition is pathological and is called transudation. An accumula- 
tion of transuded fluid in the interstices of the tissues is called oedema ; 
in the serous cavities, dropsy. Its occurrence is usually dependent 
upon some hindrance to the venous circulation or upon some change 
in the condition of the blood, which may become more watery or lead 
to alterations in the walls of the blood vessels. A simple interference 
with the outflow of lymph does not usually alone suffice to induce trans- 
udation, although it may favor its occurrence. The transuded fluid is 
usually transparent and colorless or yellowish ; it contains the same 
salts as the blood plasma, but less albumen. It may contain fat, mu- 
cin, urea, biliary acids, coloring matter of the bile ; flbrinogen is usu- 
ally present in variable quantity, and rarely fibrin. It may contain 
endothelial cells from the lymph spaces, and a variable number of red 
and white blood cells. The amount of fluid which may accumulate 
in the tissues varies greatly, depending upon whether they are loose 
or dense in texture. The flbres and cells of loose tissues may be 
crowded widely apart ; the cells are apt to be more granular than 
normal and may be atrophied. Transudations occurring in inflam- 
mation usually contain a considerable number of white blood cells and 
more or less fibrin, and difl'er in this from the non-inflammatory trans- 
udations ; but there is no sharp distinction in some cases betwet^n 
them. The inflammatory transudations are often called exudafioiis. 

THROMBOSIS AND EMBOLISM. 

Throinhosis. — Thrombosis is a coagulation of blood in the heart or 
vessels during life. The coagulum is called a tJn'ombus. Thrombi 



60 . CHANGES IX THE 

may lie against the wall of a vessel, only partially filling the lumen, 
and are then called j^cirietal thrombi ; or they may entirely fill the 
vessel, and are then called obliterating thrombi. 

Thrombi may occur as the result of an injury to the wall of a ves- 
sel, or ma.y follow its compression or dilatation ; they may result from 
some alteration of the wall of the vessel by disease or by the retarda- 
tion of the circulation. So long as the endothelial linings of the ves- 
sels are intact, simple retardation of the circulation does not usually 
alone suffice to induce coagulation ; but changes in the endothelium 
from a great variety of causes, such as inflanmiation, degeneration, 
atheroma, calcification, and the presence of tumors and foreign bod- 
ies, favor its occurrence. 

Thrombi may be composed of fibrin and of red and white blood 
cells, intermingled in about the same proportion as in an ordinary ex- 
tra vascular blood clot. These are called red thrombi, and usually 
occur from some sudden stoppage of the circulation. Other thrombi, 
usuallv such as form while the blood is in motion, mav consist almost 
entirelv of white blood cells ^vith a little fibrin, or of these intermin- 
gled Avith blood plates, or they may consist almost entirely of blood 
plates; all of these forms are called luhite thrombi. Red thrombi, 
when decolorized by changes in the blood pigment, ma}' somewhat 
resemble genuine white thrombi. Mixed thrombi are usually lamel- 
lated and contain varj'ing proportions of fibrin and red and white 
blood cells. 

The chanores which occur in the thrombus after its formation mav 
be either in the direction of degeneration or organization. In some 
cases it seems to undergo a simple shrinkage and decolorization. 
The leucocytes, the fibrin, and the blood j^lates may degenerate, 
forming a granular material which may become infiltrated with salts 
of lime, forming the so-caRedjjh I eboliths, or veinstones; in other 
cases the thrombi may soften and disintegrate. Certain thrombi 
contain bacteria or other infectious material, and on softening of the 
thrombus these may be carried into the circulation, producing very 
disastrous results. FinaUy, the thrombus may be replaced b}' a new 
formation of vascular connective tissue, itself disappearing as the 
new tissue is formed. This is called organization of the throinbus, 
but in realit}^ the new connective tissue is produced, in large measure 
at least, not from the cells of the thrombus itself, but from the cells 
of the walls of the affected vessel, from whose vasa vasorum the 
new blood vessels of the thrombus also arise. In this Avay the ves- 
sel may be completely and permanently occluded, or, more rarely, a 
channel may be re-established through the new connective-tissue 
mass. 

Thrombi in veins may lead to hyper^emia and oedema ; in arteries, 



CIRCULATION OB" THK BLOOD. 01 

to an ansemia whose significance will vary greatly, depending upon 
the situation of the occluded vessel. ^ 

Emholism. — This is the stoppage of a blood vessel by the arrest 
in its lumen of some material carried along in the circulating blood. 
The substance causing the stoppage is called an embolus. This may 
be composed of a great variety of substances. The most common 
emboli are detached portions of thrombi,- and these may have all the 
variety of structure which thrombi present. Masses of bacteria or 
other parasites, fragments of the heart valves and of tumors, drop- 
lets of fat from the medulla of fractured bones, masses of pigment, 
bubbles of air, etc., may form emboli. Embolism is, in a majority of 
cases, confined to the arteries and to the branches of the portal vein. 

The primary effect of the stoppage of an arterial trunk is, of 
course, to largely deprive the region of the body to which its branches 
are distributed of its normal supply of blood. If the branches of the 
occluded artery form anastomoses with other arteries beyond the 
point of stoppage, a collateral circulation may be established and the 
embolus do no harm. If, however, the occluded vessel be a so- 
called terminal artery — that is, one whose branches do not form 
anastomoses with other arteries — the result of the embolism is quite 
different. When a terminal artery is occluded by an embolus the 
tissue of the affected region usually dies, and there may be an extra- 
vasation of blood by diapedesis, leading to the formation of a dark- 
red, solidified area, called a hcemorrhagic infarction.^ The area of 
infarction corresponds to the region supplied with blood by the oc- 
cluded vessel, and is usually more or less wedge-shaped. 

After a time the infarction becomes decolorized, inflammatory 
changes may occur in its periphery, the blood and involved tissues 
may undergo degeneration and be absorbed, and finally the seat of 
the infarction may be indicated only by a mass of cicatricial tissue, 
which frequently contains more or less pigment. 

^ Consult Beneke, " Die Ursachen der ThrombusorganizatioD," Ziegler's Beitr. zur 
path. Anat., etc., Bd. vii., p. 158, 1889. 

'^ When an embolus lodges in a terminal artery, and the circulation in the territory 
supplied by its branches ceases, the pressure from the side of the artery is reduced to 
zero ; but, on the other hand, according to Cohuheim, the venous pressure now 
makes itself felt in a backward direction, and the capillaries and small veins in the 
affected region become crowded with blood. This blood is stagnant, however, and 
llie walls of the small vessels, being deprived of their usual nourishment, undergo, it 
is believed, degenerative changes which favor the occurrence of extensive diapedesis. 
Thus, in the hajmorrhagic infarction, not only the blood vessels but the extravascu- 
lar tissues also are crowded with stagnant blojd. Tlie researches of Litteu make it 
seem probable that, in most cases, the back pressure in the region of infarction comes, 
not from the veins, or not from them a.h)ne, but from adjacent arterial twigs which 
communicate with the capillaries of the affected region. 



62 CHANGES IX THE CIRCULATION OF THE BLOOD. 

In another class of cases, instead of an extravasation of blood in 
the affected region, the tissue is simply deprived of nourishment and 
undergoes necrosis. The affected area is then usually light in color 
and is called a tvJiite infai^ction. Inflammatory changes may occur 
in its periphery and a new connective-tissue capsule form around it, 
and the dead mass may thus persist for some time, or be gradually 
absorbed and replaced by cicatricial tissue. The scope of this book 
does not permit us to consider the somewhat complicated and often 
obscure reasons why in one case we have h?emorrhagic, in another 
white infarction, as a result of embolus. 

If the embolic material consists of or contains infectious sub- 
stances, such as some forms of bacteria, in addition to the mechani- 
cal effects of simple emboli we may have gangrene, suppuration, and 
formation of abscesses, etc. , as the result of the local action of the 
infectious material, even though this may be present in very small 
amount. 

The organs in which embolic infarctions most frequently occur 
are the spleen, kidney, brain, lungs ; less frequently the retina, liver, 
and small intestines. Hsemorrhagic infarctions are not liable to oc- 
cur in the Hver from emboH in the branches of the portal vein, on 
account of the blood supply v/hich may come to the affected region 
through the branches of the hepatic artery. On the other hand, em- 
bolic abscesses from infectious emboli are of not infrequent occur- 
rence here. Hsemorrhagic infarctions may occur exceptionally in re- 
gions not furnished \\ath terminal arteries, as in the small intestines. 



CHANGES I2s^ THE COMPOSlTiOE" AXD 
STEUCTUEE OF THE BLOOD. 



Only the more common morphological alterations of the blood 
will be considered here, and particularly such as may be appreciable 
after death. ' 

The coagulability of the blood and the characters of the result- 
ing clot vary widely, depending partly upon the composition of 
the blood and partly upon the conditions under which the coagula- 
tion occurs. There may be very little coagulation of the blood in 
death from the exclusion of air from the lungs, or from diseases 
and accidents which in any way interfere with the aeration of the 
blood and permit the accumulation of carbonic acid within it. Thus, 
in death from strangulation or drowning, many chronic diseases, 
scurvy, and under many conditions which we do not understand, the 
blood may remain fluid, or nearly so, after death. On the other 
hand, in a variety of acute inflammatory diseases, such as rheuma- 
tism, pneumonia, etc. , very voluminous clots may be formed, although 
this is by no means constantly the case. The fact that large clots 
form after death is not conclusive evidence that an undue amount of 
fibrin-forming elements were present in the blood, nor does the ab- 
sence of marked coagulation prove a diminution in the blood of 
fibrin-forming elements. 

The blood may be very thick from the removal of its fluid con- 
stituents in diseases associated with excessive serous discharges 
from the intestines. It is especially marked in some cases of cholera, 
and is called anhydrcemia. On the other hand, the blood may con- 
tain a large amount of water in proportion to its solid ingredi- 
ents — albumen and blood cells. This is called hf/di'cvmia, and occurs 
in a variety of diseases of the heart, kidneys, liver, and lungs. 

Owing to the destruction of red blood cells in some forms of poi- 
soning, burning, etc., the blood plasma may contain free liiBmoglobin. 

' For a resume with bibliography of the more receut studies ou the origin of 
blood cells, see OpjJcl, Centralblatt fi'ir allg. Pathologie. etc.. Bd. iii., Xo3. 5 and 
(i, 1892. 



64 CHANGES IX THE COMPOSITION 

by which it is discolored {hcenioglobinceniia), or it may be stained 
from the absorption of bile pigment. 

The blood may be actually increased in amount (plethora), usually 
temporarily only ; or by actual loss of blood, as in hsemorrhage, it 
may be diminished in amount (oligsemia). 

AX.^MIA. 

In general, ancemia means a diminished quantity of blood or of 
red blood cells in the vessels of the whole or a part of the body. 
Anaemia may be secondary to hsemorrhages, to prolonged innutrition, 
to chronic organic diseases of many kinds tc the action of poisons, to 
functional disturbances of an unknown nature in the blood-forming 
apparatus, and to wholly unknown causes. For a consideration in 
detail of the varying degrees and forms and causes of anaemia we 
must refer to works on the 23ractice of medicine or clinical raicro- 
scopy. Fatty degeneration of the heart and blood vessels, liver, 
kidney, etc., and capillary haemorrhages and a change of the yeUow 
into red marrow, are frequent accompaniments of excessive anaemia. 
This latter change is largely due to the disappearance of the fat. 
Nucleated red blood cells are also observed in the red marrow. 

CHANGES IN THE RED BLOOD CELLS. 

These may be diminished in number and may undergo various 
changes in shape and size and structure. 

Oligocythcemia is that condition of the blood in whicli the num- 
ber of the red cells is reduced. This reduction in number may be 
temporary, as after haemorrhage, or it may be persistent in some 
forms of anaemia and in leukaemia, in inanition, and in various infec- 
tious diseases. The number of red blood cells may in extreme cases 
of anaemia be reduced to one-tenth of the normal, or even less ; that 
is, from the normal number, which is between four and five million, 
there may be a reduction to half a million or less. 

The red blood cells may, in addition to a decrease in numbers, 
contain less than the normal amount of haemoglobin. The blood as 
a whole may be pale and watery in appearance. 

Under a variety of conditions in profound anaemia, after certain 
forms of poisoning, severe burns, etc. , varying numbers of spheroidal 
or irregular-shaped bodies, smaller than the red blood cells but hav- 
ing the same general color and characters, may be found in the blood. 
These are called microcytes. In pernicious anaemia and in leukaemia 
red blood cells larger than the normal — macrocijtes — may be found in 
the blood. Under similar conditions a variety of bizarre forms of 
red cells are found, which are QRWeiS. poikiloGytes. 



AND STRUCTURE OF THE BLOOD. 05 

In profound anaemia and in leukaemia nucleated red blood cells, 
either of normal size or larger, may be found in the blood. 

Under the varying conditions associated with these changes in 
the red blood cells the leucocytes may remain in normal proportion, 
or they may be increased in number or be otherwise changed. 

CHANGES IN THE WHITE BLOOD CELLS. 

Recent studies have shown that among the colorless blood cells 
which we have been accustomed to speak of indiscriminately as leu- 
cocytes there are several varieties. We may distinguish in normal 
human blood — 

1. Small cells about as large as the red blood cells, with a single 
large, easily stained nucleus surrounded by a narrow rim of proto- 
plasm. These are called small lymphocytes. 

2. Larger mononuclear cells — large lymphocytes — with a much 
greater relative amount of protoplasm, the nucleus staining less 
deeply than in the smaller lymphocytes. The lymphocytes appear to 
come from the lymph nodes. 

3. Cells having a single nucleus of an irregular shape and pre- 
senting intermediate forms between the lymphocytes and the poly nu- 
clear forms. 

4. Cells somewhat smaller than 'No. 2, with several much-con- 
torted nuclei which are readily stained. The protoplasm of these 
cells usually contains granules which comport themselves in a pecu- 
liar way toward certain staining agents. They are colored by neu- 
tral stains. These cells are accordingly called polynuclear neutro- 
phile leucocytes. 

5. Finally, there are cells having one or two, and more rarely 
three, easily stained nuclei, the protoplasm containing granules 
which are stained by such an acid coloring matter as eosin. These 
cells are accordingly called eosinophile leucocytes. Their granules 
are in general larger than those of the neutrophile cells. 

These various forms of cells occur in the blood inider normal con- 
ditions in fairly constant proportions to one another. The polynu- 
clear neutrophiies make up about from sixty to seventy per cent of 
the leucocytes, the lymphocytes are next most abundant, while the 
eosinophiles are normally present in a smaller percentage still, vari- 
ously stated as from two to ten per cent. 

A large number of variations in the size and form of both the red 
and white blood cells have been described, and various classitieatious 
have been suggested, based either upon morphological characters or 
the effects of staining agents. ]Mucli stress has furthermore been 
laid by special workers in this field upon the relationship of some of 
these forms to varying phases of disease. But since a good deal of 



66 



CHANGES IX THE COMPOSITION 



diversity of opinion still exists in regard to the significance, and even 
the number, of varying forms of blood cells, both in health and dis- 
ease, we have deemed it best to give here only a resume of the more 
general and definitely known facts. ' 

The leucocytes may be increased in number, and this increase may 
be temporary or persistent. 

Leucocytosis signifies a temporary increase in the number of 
white blood cells, largely of the polynuclear form. This increase is 
usually of moderate amount, but may be extreme. It occiu"s in a 
variety of acute infiammatory diseases, in typhoid fever and acute 
lobar pneumonia, in profuse suppui-ation in any part of the body, 
often in connection with mahgnant tumors, tuberculosis, etc., and 
may, as above stated, be associated ^vith anaemia. 

This pathological leucocytosis should not be confounded ^vith the 
physiological leucocytosis which regularly occurs during diges- 
tion, and during which the relative proportion between red and 
colorless blood cells may be 1: 150 or 1: 100, whereas in health, under 
other circumstances, the proportion is usually from 1:335-600 or 
thereabouts. In young children the relative number of leucocytes is 
greater. 

Leukcemia {Leucocythcemia). — This disease is characterized by a 
persistent, progressive, and often enormous increase in the number of 
the white blood cells. The blood is pale in well-marked cases, but 
not watery, and the number of white blood cells may in extreme cases 
equal or even exceed that of the red. But the mere statement of a 
numerical increase in leucocytes does not express all our knowledge 
in this matter. 

While in leucocytosis it is largely the polynuclear cells, as stated 
above, "which are increased in nmnber, in leukcemia the case is not so 
simple. In hinphatic leukaemia (see General Diseases) the increase in 
the number of leucoc}i:es is due to the mononuclear hmiphocytes, espe- 
cially of the small form. As many as ninety-five per cent of the 
colorless cells may be of this form. In splenic-myelogenous leukgemia 
the eosinophile cells may be especially increased in number, and there 
are also large leucocytes coming apparently from the marrow of the 
bones, and called myelocytes. These most nearly resemble the larger 
lymphocytes of normal blood, but they are usually larger. They 



^ We refer, for details of methods of quantitative determination of changes in the 
chemical and morphological constituents of the blood, to special works on the blood, 
such as Von Limbeck, ''Grundriss einer klinischen Pathologie des Blutes," 1892, in 
which a full bibliography will be found, including the numerous and valuable re- 
ports of Ehrlich, and Hayem, " Du Sang," 18S9; and to works on clinical microscopy — 
VonJaksch, "Clinical Diagnosis," 3d ed., 1892; Bizzozero, " Clinical Microscopy." 



AND STRUCTURE OF THE BLOOD. 67 

have a single large nucleus, which stains feebly, and their bodies may 
show neutrophile granules. Larger and smaller nucleated red blood 
cells may be found in splenic-myelogenous leuksemia. 

The leucocytes are frequently in a condition of fatty degeneration, 
and there may be a decrease in the number of red blood cells in leuco- 
cythiiemia. There are marked changes in the liver, spleen, and lymph 
nodes, as well as in the bone marrow, in leuksemia ; the degree of 
involvement of the different organs varying in different cases (see 
Leuksemia, in section devoted to General Diseases). 

Most of the above-mentioned changes in the morphological char- 
acters of the blood are better studied during life than after death, 
since the redistribution of its elements, owing to the clotting and the 
effects of gravity, renders the obtaining of a pure sample very diffi- 
cult or impossible and the results of examination only in a very 
general way reliable. 

Melancemia. — In this condition the blood contains larger and 
smaller irregular-shaped particles or masses of brown or black pig- 
ment. This condition is most frequently the result of intermittent 
and remittent fever, particularly the severer forms. It may be ac- 
companied by ancemia and leucocytosis. It does not occur in all cases 
of the above-named affections. It may be transient in character. 
The pigment may be free, or more usually is enclosed in leucocytes. 
Under the same conditions pigment may be deposited in the Hver, 
spleen, lymph nodes, bone marrow, and blood vessels. Owing to 
the deposit of pigment in the organs they may assume a gray or slate 
color. The pigment is supposed to originate in the decomposition of 
the hsemoglobin. Pigment which has been taken into the lungs from 
the air, such as coal dust, etc. , may find its way into the blood either 
before or after deposition in the bronchial or other lymph nodes, and 
may be afterwards deposited in the spleen and liver. 

METHOD OF EXAMINATION OF THE BLOOD. 

The blood may be examined fresh on the warm stage without the 
addition of any fixative, simply surrounding the cover with oil or 
vaselin to prevent evaporation. For most purposes, however, the 
cells should be treated in some way, so as to retain their normal 
form, the instant the blood leaves the vessels. This fixation may be 
accomplished by the use of chemical agents (wet method) or by quick 
drying on the cover glass or slide (dry method). 

Wet Method. — Among the chemical fixative agents are osniic 
acid and a solution of corrosive sublimate. Osmic acid : A drop or 
two of blood drawn from the cleansed finger tip by a needle prick is 
allowed to fall into a cubic centimetre of from one- to two-per-cont 
osmic acid. After an hour the blood colls mav be transferred bv a 



68 CHANGES IN THE COMPOSITION 

pipette to a solution of acetate of potash, in which they may be pre- 
served. Sublimate may be used in the form of Hayem^s solution : 

Hayeiivs Solution. 

Chloride of Sodium 1 gm. 

Sulphate " '' 5 

Corrosive Sublimate 0. 5 ^^ 

Water, distilled , 200 " 

The blood is received directly into this solution, in which it is 
studied. 

Dry Method. — It has been found that if the freshly drawn blood 
from a finger prick be immediately dried on glass in a very thin 
layer, the cell forms are quite well preserved and may be exposed to 
the action of staining agents, by which many features are developed 
not easily seen by the wet method. For this purpose perfectly clean 
cover glasses should be used. One cover should be touched to the 
blood droplet, taking up a very small portion, and instantly another 
cover, or the edge of a spatula or the side of a needle, is drawn 
quickly across the drop. In this way a uniform layer of blood is 
spread over each cover, which instantly dries. 

For a simple staining of red and white blood cells the following 
procedure gives good results and is sufficient for most practical 
purposes : 

The covers, prepared by drying the blood on them, are heated for 
ten minutes at from 110° to 120° C.;^ or, though less to be recom- 
mended, they may be kept for ten minutes in a mixture of equal 
parts of alcohol and ether to fix the haemoglobin and to render the 
albuminates insoluble. They are then floated, specimen side down, 
for ten to fifteen minutes with gentle heat in the following fluid 
(Czenzynski^s) : 

Aqueous Methyl Blue, saturated solution 40 c.c. 

One-half -per-cent solution of Eosin in seventy-per- 
cent Alcohol .20 " 

Water .40 " 

The red cells and eosinophile granulations are in this way colored 
red, while the cell nuclei of the various forms of leucocytes are blue. 
The neutrophile granules are not stained. By this method the Plas- 
modium malarise may also be stained blue. 

^ A convenient method of heatin g such specimens is to lay them near the end of a 
strip of copper either held in a clamp or resting on a wire loop, and heated at the 
opposite end by a lamp. A little preliminary observation with a thermometer will 
suffice to locate the proper position for the specimens. Or a regular closed air bath 
may be used. 



AND STRUCTURE OF THE BLOOD. GO 

The more elaborate methods of differential staining of leucocytes 
devised by Ehrlich and others need not be considered here in detail. 
But the method of Ehrlich for the demonstration of the neutrophile 
granulations in the polynuclear leucocytes, which are increased in the 
blood in leucocytosis and emigrate from the vessels in exudative in- 
flammation, is as follows : 

The blood is fixed in either of the above ways on the cover glass 
and stained in the color mixture prepared as follows : 

Saturated aqueous solution of orange G 125 c.c. 

Saturated aqueous solution Acid Fuchsin con- 
taining 20 per cent of alcohol 125 



a 



To this mixture, with constant stirring, are added 125 c.c. of satu- 
rated aqueous solution of methyl green and 75 c.c. absolute alcohol. 

This mixture must stand for some time before using. 

For use it must not be filtered, but a drop, taken out in a pipette or 
on a rod, is put on to the blood-smeared cover glass, fixed as above 
described, and allowed to act for a few moments, while the cover is 
tilted back and forth so that the solution shall not dry on the glass. 
The excess of stain is now rinsed off with water and the specimen 
dried and mounted in balsam. The nuclei are of a greenish-blue or 
bluish- violet color ; the neutrophile granules are grayish or reddish 
violet ; the eosiiiophile granules are yellowish-red or dark-red, while 
the red blood cells are orange-yellow. This solution is somewhat im.- 
certain in its action, often changing and j^resenting variations in its 
coloring power. ^ 

FOREIGN BODIES IN THE BLOOD. 

Various bodies which do not belong there, aside from those above 
mentioned, may find access to the vessels and mingle with the blood. 
Pus cells may get into the blood from the opening of an abscess into 
the vessel or from some inflammatory change in its walls. Desqua- 
mated endothelial cells from the vessel walls, either in a condition of 
fatty degeneration or in various stages of proliferation, may be min- 
gled with the normal blood elements ; also tumor cells of various 
kinds, fragments of disintegrating thrombi, portions of heart valves, 
etc. Crystals of bilirubin have been found in the blood in icterus. 

Fat, in a moderate amount, is a normal ingredient of the blood 
during digestion and in lactation. Under pathological conditions it 
may occur in larger and smaller droplets. This lipcvmia occurs as 
a result of deficient oxidation, in diabetes, in drunkards, and in some 

^ For various other methods of staiuiug blood cells, aud for detailed consideration 
of morphological changes in disease, we refer to Von Limbt'ck, **Klin. Pathologie 
desBlutes," 1892. 



70 CHANGES IN THE COMPOSITION AND STRUCTURE OF THE BLOOD. 

cases of dyspnoea from various causes. The droplets are small and 
liable to escape observation. 

In many cases of injury, particularly in crushing fractures of the 
bone, the fat of the marrow finds its way into the blood, and it may 
coUect in large drops in the vessels of the lungs, forming the so- 
called, fat emboli j or it may pass the lungs and form emboli in other 
parts, as the brain, kidneys, etc. Fat embolism in eclampsia is of 
occasional occurrence. 

" The fat may be absorbed from the vessels, ha^ang produced little 
or no disturbance ; or in some cases it may produce serious results by 
the stoppage of a large series of vessels in the lungs, brain, or other 
parts of the body. ^ 

The fat may be best seen by cutting sections of the fresh tissues 
with the freezing microtome and staining them at once for twenty- 
four hours with one-per-cent aqueous solution of osmic acid. They 
may then be mounted in glycerin. 

Air in the blood, as the result of an opening in the veins, is of 
occasional occurrence. If the amount of air be small it appears to 
be readily absorbed and does httle or no harm. If, on the other 
hand, a large quantity is admitted to the veins at once, it collects in 
the right side of the heart, from which the contractions of the organ 
are unable to force it in any considerable quantity, and, the supply 
of blood being thus cut off from the lungs, death very quickly en- 
sues. It is especially from wounds of the veins of the neck and 
thorax that the accident is most apt to occur. But it may be due to 
the introduction of air into the uterine veins in intra-uterine injec- 
tion or in the removal of tumors. ^ 

The occurrence of animal and vegetable parasites is considered 
more in detail in parts of this book devoted to these organisms. It 
will suffice to mention here that the more important of the animal 
parasites of the blood are : the Filaria sanguinis hominis, the Dis- 
toma hcematobium, and the embryos of trichina and echinococ- 
cus, which are of occasional and usual temporary occurrence. 

The various species of bacteria which may be found in the blood 
will be considered in parts of this book in which these organisms are 
treated in detail. 

^ Consult for resume of this subject, with good bibliography, article by Park oa 
"Fat Embolism," New York Medical Journal, August 16th, 1884. 

2 Consult Couty, "Etudes exp, sur I'entree de I'air dans les veines," Paris, 1875, 
for experiments and older literature ; also later article by Couty, Arch, de Physiol, 
nor. et path., 2d ser., t. ir., p. 439, 1877; more recent consideration of the subject la 
Archiv fiir klin. Medicin, Bd. xxxi., p. 441, 1882, by Jilrgensen. 



HYPERTROPHY, HYPERPLASIA, REGEll^E- 
RATIO:Nr, METAPLASIA. 



HYPERTROPHY AND HYPERPLASIA. 

Under a variety of conditions parts of the body or organs be- 
come larger than normal — hypertrophied. "When we look for the 
structural changes to which hypertrophy is due, we find that it may 
be owing to a simple increase in size of the elementary structures 
of the part, cells, and other tissue elements. This is called simple 
hypertrophy. 

On the other hand, it is found in many cases that the increase in 
size of a part or organ is due not only, or not at all, to the increase in 
size of its elementary structures, but to an increase in their number. 
This increase in number of the structural elements of a tissue or 
organ is called numerical hypertrophy, or hyperplasia. 

Simple hypertrophy and hyperplasia are frequently associated. 

REGENERATION, 

The wear and tear of the body in the performance of its varied 
functions and labors, and the greater or smaller injuries to which it 
is frequently exposed, make indispensable for the maintenance of its 
integrity a more or less constant and widespread regeneration of 
tissue. 

This regeneration of injured or worn-out tissues, all new growths, 
as well as the hyperplasias above mentioned, are invariably brought 
about by proliferation or other changes in living cells. 

A new formation of cells in the body, so especially characteristic 
of this period of development, thus persists through life with var^'ing 
degrees of activity. It is in the adult, however, under pathological 
conditions — in the course of inflammation in the growth of tumors — 
that those cell proliferations occur which especiall\' concern us here. 

Just as the cells of the adult organism are the offspring of one 
original cell, the ovum, so are all the now cells which appear in the 
body under abnormal conditions derived from some pre-existing colls 
by a division of their bodies. 



72 HYPERTROPHY. HYPERPLASIA, 

The careful and minute study of cells during the act of di^T.sion, 
which has been recently made, has reYcaled many most curious 
phenomena and has opened a new world of observation nearer to 
the elementary expression of hf e than has seemed possible in earlier 
times. It will suffice for our purposes to briefly indicate some of 
the more striking features of the new cell lore. 

The earliest morphological changes in cell di\dsion are seen in the 
nucleus. 

Direct {Amitotic) Cell Division. — In what to-day appears to 
be the most simple mode of cell division — and this was formerly the 
only one recognized — the nucleus with its membrane becomes con- 
stricted and finally divides into two or more parts which become new 
nuclei. Hand-in-hand with or following this simple nuclear division 
the cell body divides, and thus two or more cells may form in the 
place of one. Sometimes the nuclear division is not followed by a 
division of the cell body, and thus multinuclear cells may be formed. 
Whether in this mode of cell di\^sion there ma}" not be as yet unre- 
cognized minute changes in the cell nucleus, ushering in the process, 
seems not to be altogether clear. 

Indirect {Mitotic) Cell Division. — In this mode of cell multi- 
phcation certain minute changes in the nucleus usher in the coarser 
process of di^'ision. The earlier changes which are to be seen in a 
cell about to divide are a thickening and rearrangement of the gran- 
ules and fibres of the intranuclear network^ (Fig. 4; 1 and-?). As 
these granules and fibres of the nucleus become thicker they arrange 
themselves into an irregular snarl or contorted mass, the nucleolus 
disappears, and the nuclear membrane becomes indistinct (Fig. 4 ; ^). 
^ow the thickened fibres of the nucleus may arrange themselves in 
varying stellar forms and separate into two or more groups, which 
slowly draw asunder (Fig. 4 ; Jf, 5, and 6). Then the cell body 
shows commencing constriction corresponding to the division of the 
nuclear fibre masses (Fig. 4; 7). Finally a nuclear membrane de- 
velops around each of the new nuclei, their fibres become more 
slender and assume the resting arrangement, and the cell body com- 
pletes its di\4sion by a deepening of its constriction (see Fig. ^\ 8 and 
9). There are countless variations and details in the minute process 
of cell division which we need not consider here. 

The term mitosis or kar y omit o sis is applied to this indirect mode 
of cell division on account of the involvement of the nuclear threads. 
It is also sometimes designated as karyokinesis, from the form 
changes which these threads undergo. Aside from its intrinsic bio- 
logical interest, a knowledge of mitosis in proliferating cells is of im- 

' This solid and stainable part of the nucleus is comnioaly called chromatin. 



REGENERATION, METAPLASIA. 73 

portance in pathology, because the recognition of mitotic figures often 
enables us to decide with certainty what particular cells or cell 
groups are involved in the formation of new tissue. 

It is not necessary for us to follow in detail here the processes of 
regeneration and repair in the different tissues and organs. It should 
be borne in mind that individual cells maj^, even after having under- 
gone marked structural changes — as, for example, in acute granular 
degeneration — be restored to a perfectly normal condition. 

After injury or loss a full and complete regeneration of cells and 
tissues can occur only as the result of a proliferation of cells of the 
same type as those to be restored. Thus a regeneration of epithelium 
occurs by proliferation and growth of epithelial cells alone ; regene- 



i 









%' 






'^^^.^' '"^^^si^^ ^^^^^^ 

/ 1 3 



mmm 



^i'frmiM 



0MM i'|*l Isfli 
^£-^m'a V:'::%m m^^4 









,x 



if 






? 






:0 



-<»<*.tj»<,r' 



■-''^jWS* 



i 

Fig. 4.— Phases of Mitosis, or Indirect Cell Division. 

ration of muscle by muscle cells ; of nerve by nerve cells, etc. In 
fact, however, in the higher types of tissue, after considerable injuries 
with loss of substance or after destructive pathological processes, 
complete regeneration is not common. This is because the liighly 
specialized cells of the body are limited in their capacity for repro- 
duction closely to the domain of physiological regeneration. 

What we ordinarily call healing, in extensive wounds of the more 
highly specialized tissues, is usually a provisional makeshift repair by 
means of new-formed connective tissue. Such regeneration as takes 
place in nerves after partial destruction is brought about by prolifera- 
tion of (H^lls of the nerve fibres themselves, but it is a fibrous-tissue 
healing only which is possible, when loss of tissue is extensive. And 



74 HYPERTROPHY, HYPERPLASIA, 

it is this alone which, after large injuries to the brain, achieves a 
patchwork repair. 

In injuries of muscle, too, the remains of muscle protoplasm may 
undergo proliferation in moderate degree and lead to a partial resti- 
tution of muscle tissue. This, however, is usually atypical in struc- 
ture and of little functional importance. Losses of substances in 
muscle are largely repaired, with varying functional success, by 
connective tissue. 

Specialized gland tissue, while readily enough maintaining by cell 
proliferation its integrity under the ordinary functional wear and 
tear, is incapable, by proliferation of its specially endowed cells, of 
making good extensive losses of substance, either from injury or de- 
structive pathological processes. It should not be understood by this 
that healing and a general restoration of the part may not occur after 
extensive injuries to such organs as the liver, kidney, thyroid gland, 
etc. ; such a general healing may occur, but it is largely through 
growth of new connective tissue. The specialized gland cells, be it 
in the liver, kidney, salivary, or other glands, or in the mucous mem- 
branes, under favorable conditions are apt to respond to an injury 
with destruction of tissue by proliferation, or, it may be, by the 
actual production of considerable new gland tissue. But the new 
gland tissue thus produced is usually inconsiderable in amount, 
atypical in form, and of questionable functional value. 

We thus see that though specialized cells in the body express, in 
the face of tissue injuries, distinct recuperative tendencies^ they are 
not in general able to make good extensive losses of substance. This 
is done by the cells of a group of tissues more lowly in organization, 
but retaining largely the proliferative power of undifferentiated pro- 
toplasm. 

The formation of leucocytes appears to occur chiefly "in those 
masses of lymphoid tissue which are so widely scattered in the body 
in the lymph nodes, in the spleen, and in the walls of the gastro-in- 
testinal canal. 

Both mitotic and amitotic cell division are to be observed in the 
new formation of leucocytes, but the exact relationship between the 
new cells produced in these two ways, and their respective destinies, 
is not yet very clear (see Blood). 

Regeneration of red blood cells seems to occur in the bone marrow 
through mitotic division of nucleated forms. The latter may, under 
pathological conditions, appear in the vessels in varying numbers. 

METAPLASIA. 

The members of the connective-tissue group — fibrous tissue, mu- 
cous and fat tissue, cartilage, bone, etc. — are so closely related in 



REGENERATION, METAPLASIA. 75 

nature and structure that not infrequently and under a variety of 
conditions one form of tissue will assume the characters of another. 
This change of one form of tissue into another is called metaplasia. 
Thus, by a gradual change in the cells and stroma of fibrous tis- 
sue this may be converted into bone, as mucous tissue may become 
fat tissue, and hyalin cartilage become fibrous. Metaplasia is a 
process involving active changes on the part of the living cells of the 
tissue, and should be clearly distinguished from certain degenera- 
tive processes, in the course of which one form of connective tissue 
may assume superficial resemblances to others of the group, as in 
calcareous and mucoid degeneration. While metaplasia is most 
common among the members of the connective-tissue group, it some- 
times occurs in other tissues. Thus, for example, under certain con- 
ditions one type of epithelium may assume the morphological charac- 
ters of another. 



DEQEl^EEATITE OHAISTaES IN THE TISSUES. 



Necrosis. — N"ecrosis is the death of a circumscribed portion of 
tissue. It may be the result of insufficient nutrition from the cut- 
ting-off of the blood supply ; or it may depend upon the action of 
destructive chemical agents, extreme degrees of temperature, certain 
materials produced by the life processes of some forms of bacteria ; 
or it may be due to mechanical injury. The appearances which dead 
tissues present under the microscope vary greatly. In some cases 
we have a simple and gradual disintegration and softening of the 
tissue, resulting in a mass of degenerated cells and cell detritus, 
with more or less fluid and various chemical substances arising 
from decomposition. The softening of the brain in embolism is an 
example of simple necrotic softening. In some cases the dead tissues 
simply gradually dry and shrivel and become hard and dark colored. 

In another class of cases the dead tissues are permeated by fluids 
which may be dark red in color from the solution of coloring matter 
from the blood, and contain bacteria which induce putrefaction with 
the production of gases and various new chemical substances. The 
tissues become swollen and granular, and disintegrate ; and finally 
the whole may form a mass of irregular granules with fat droplets, 
various forms of crystals, shreds of the more resistant kinds of tis- 
sue, and bacteria. 

Coagulatio7i Necrosis. — If the supply of blood is shut off from a 
portion of tissue which is surrounded by, or continuous with, other 
tissue in which the blood continues to circulate, there results a death 
and transformation of a peculiar character. The composition of the 
cells of the tissue is altered, so that the cell bodies are shining and 
translucent, diminished in size, sometimes altered in shape, and the 
nuclei of the cells disappear. The white infarctions of the spleen 
and kidneys, the areas of coagulation necrosis in tuberculosis, and 
the pseudo-membrane in croupous inflammation of the mucous mem- 
branes are the most common examples of this lesion. 

If, for example, in the spleen, one of the small arteries is plugged 
by an embolus, a corresponding portion of the spleen becomes anse- 



DEGENERATIVE CHANGES IN THE TISSL'ES. 



77 



mic and appears as a white, wedge-shaped mass, sharply defined 
from the surrounding splenic tissue. If such a white infarction has 
existed but a short time there is hardly any difference between the 
appearance of its anatomical elements and those of the surround- 
ing spleen, except that they are differently affected by staining fluids. 
If the infarction is older the cells are small and shiny and their 
nuclei cannot be seen. 

In croupous inflammations of mucous membranes the epithelial 
cells become shiny, the nuclei disappear, and the shape of the cells is 
changed by the coagulation necrosis, so that a number of them to- 
gether often look like a network of coagulated fibrin. 

Cheesy Degeneration. — As commonly used this term embraces 
the changes in the tissues which we have just considered under the 
more appropriate name of coagulation necrosis. But it is also and 
more properly applied to that form of degeneration in which, under 



:'"-'MmW--^'^^-^-'^'Mt''^w'^4 






Fig. 5.— Cheesy Degeneration (Coagulation Necrosis) in Miliary Tubercle op Lung. 



a variety of conditions, the dead tissue elements lose their normal 
structural features and become converted into an irregularh' granular 
albuminous and fatty material which sometimes tends to disintegrate 
and soften, sometimes dries and becomes dense and firm, or may be- 
come infiltrated with salts of calcium. Thus cheesy degeneration 
may, and very often does, occur in tissues which are in the condition 
of coagulation necrosis; but it also occurs in tissues which are not 
the seat of coagulation necrosis, but which, for a variety of reasons 
and in a variety of ways, have lost their vitality. 

The terms coagulation necrosis and cheesy degeneration, as com- 
monly used, in part actually cover the same degenerative conditions 
in the tissues. Both are indefinite, and will no doubt remain so un- 
til we obtain a more definite knowledge of the lesions which thoy 
represent. 

Parenchymatous DegeucrafioN (Acute Degeneration: Granukir 



78 DEGENERATIVE CHANGES IN THE TISSUES. 

Degeneration; Cloudy Swelling). — In this condition the cells of tis- 
sues and organs are swollen and filled with small albuminous gran- 
ules, which may be so abundant as to entirely conceal the original 
cell structure. The granules disappear on treatment with acetic acid, 
and are insoluble in ether. This degeneration may be present in the 
parench^^xLa cells of any inflamed organ, but is most marked and fre- 
quent in the liver, kidney, heart muscle, and mucous membrane of 
■the gastro-intestinal canal. It may occur in infectious or severe 
febrile diseases, after severe burns, and in poisoning with arsenic, 
phosphorus, or mineral acids. It is often associated with various 
phases of exudative inflammation. The cells in a condition of paren- 
chymatous degeneration may regain their normal condition, or be- 
come fatty, or disintegrate. In such organs as the liver, kidney, and 
heart the gross appearances are often very characteristic ; the tissue 




Fig. 6.— Fatty Degeneration of Heart Muscle. 

is swollen and has a less translucent and more dull and grayish look 
than under normal conditions. 

The microscopical study of this lesion is best done in sections of the fresh tissue 
made with the freezing microtome, or in teased fresh tissue in one-half- per- cent salt 
solution. 

Fatty Degeneration. — This is the conversion of the protoplasm 
of cells into fat, which accumulates in the cell body. The fat is usually 
present in the cell in very small particle^ or droplets, but these may 
coalesce to form large drops. The protoplasm may even be almost 
entirely replaced by the fat. 

Fatty Infiltration of cells is a common occurrence under normal 
as well as pathological conditions. The fat is believed to originate 
outside of the cells and simply accumulate in them, causing a passive 
atrophy of the protoplasm. In this way fatty infiltration is believed 
to differ essentially from fatty degeneration, but in many cases a de- 
finite distinction between the two is impossible with our present 
knowledge of the chemistry of cell life. In general the fat droplets 



DEGENERATIVE CHANGES IN THE TISSUES. 



79 



are larger in fatty infiltration than in fatty degeneration, yet to this 
there are many exceptions. Fat granules and droplets are recog- 
nized in cells by their strong refraction, by their solubility in alcohol 
and ether and their insolubility in acetic acid, and by the black 
color which they assume when the fresh tissue is treated with osmic 
acid. IS'ot infrequently feathery clusters of delicate fat crystals 
occur within the cells. Fatty -degenerated cells may break down and 
form an oily detritus, in which, especially when much moisture is 
present, cholesterin crystals may be formed by decomposition of the 
fat. 

To the naked eye, organs in a condition of marked fatty degenera- 
tion are usually larger and softer than normal, have a grayish-yellow 
color or are mottled with yellowish strea^ks or patches, and the nor- 
mal markings of cut surfaces are more or less obscured. 




Fig. 7.— Fatty Infiltration of Liver Cells. 



Fatty degeneration may be due to local or general disturbances 
of nutrition, from a great variety of causes — disturbances which 
either directly affect the life processes of the cells themselves, or 
which produce alterations in their nutritive supply. In addition to 
its local occurrence, as a result of local disturbances of circulation, in 
the vicinit}^ of inflammations or in tumors, etc. , it is apt to occur in 
the liver, heart muscle, and kidney in chronic exhausting diseases 
and in conditions and diseases to which profound auiiemia is incident, 
or as the result of the action of certain poisons, such as phosphorus 
and arsenic. Fatty degeneration is, as a rule, a more serious lesion 
than fatty infiltration. 

Tissues in a condition of fatty degeneration or infiltration may be studied by teas- 
ing, or cutting the fresh tissue with the freezing microtome and examining unstained, 
or lightly stained with eosin, in one-half-per-cent salt solution. Or they may be 
placed, when fresh, for twenty-four hours iu one-per-ceut solution of osmic acid, and 
then studied, either after teasing or in sections, iu glycerin. A preliminary harden- 



80 DEGENERATIVE CHANGES IN THE TISSUES. 

ing in Mliller's fluid and afterward in alcohol gives moderately good results if the 
lesion is extensive. But it should be remembered that in tissues which have been 
soaked in alcohol the fat is no longer present, its former seat being indicated by clear 
spaces which are filled with the mounting medium. The fat crystals, however, often 
persist after prolonged soaking in alcohol. 

Amyloid Degeneration (Waxy or Lardaceous Degeneration). — 
This is a process by which the basement substance of various forms 
of connective tissue, and especially the walls of the blood vessels, be- 
come swollen and thickened by their conversion into a translucent, 
firm, glassy, colorless material, albuminous in character. This albu- 
minous material inay be present in the tissues in such small amount 
as to be recognizable only under the microscope, or it may be so 
abundant as to give a very characteristic appearance to the tissue. 
Parts in which the lesion is marked are usually larger and contain 
less blood and feel harder than normal, and have a peculiar dull 
shining and translucent appearance which varies in character, de- 
pending upon the extent and distribution of the degenerated areas 
and upon its association with other lesions, such as fatty degenera- 
tion. It most frequently occurs in the smaller arteries and capillaries, 
whose lumen becomes encroached upon by the thickening of the 
walls which the process involves. It is usually the media and inter- 
mediary layers of the intima which are earliest and most extensively 
affected. The change also often occurs in the interstitial connective 
tissue and membranse propriae of organs and in reticular connective 
tissue. It is both asserted and denied that it may affect .the paren- 
chyma cells of organs. We have not been able to find unmistakable 
evidence of its occurrence in parenchyma cells. These, however, 
frequently undergo atrophy as the result of pressure from the swol- 
len, degenerated tissue. 

It is not yet known whether amyloid degeneration is due to a 
direct transformation of the tissue, or is an infiltration of the tissue by 
some abnormal material formed elsewhere and brought to it, or is de- 
rived from the blood. 

Amyloid degeneration occurs most frequently and abundantly in 
the liver, spleen, kidneys, intestinal canal, and lymph nodes; but it 
m.ay occur, usually in a less marked degree, in other parts of the 
body : in the larger blood vessels, in the interstitial tissue of the 
heart and mucous membranes of the air passages, and in the genera- 
tive organs. It may occur locally or appear in various parts of the 
body at once. It may exist without any known cause, but it most 
frequently occurs in connection with severe wasting diseases, par ■ 
ticularly in those involving chronic suppuration and ulceration, espe- 
cially of the bones. It frequently occurs in tuberculosis, syphilis, 
in the cachectic condition induced by malignant tumors, and is 



DEGENERATIVE CHANGES IN THE TISSUES. 



81 



occasionally seen in severe malarial infection, dysentery, and leu- 
kiBmia. 

For microscopical examination, the tissue, either fresh or after preservation, should 
be cut into thin sections, and these deeply stained with one-per-cent aqueous solution 
of methyl violet ; the sections are washed in water and mounted in glycerin. The 
differentiation between the amyloid and other parts is more distinct if, after staining, 
the specimen be dipped for an instant in HCl and alcohol 1 : 100, and then carefully 
rinsed, before mounting in glycerin. The degenerated areas are thus stained rose-red 
(Fig. 8), while the normal tissue elements have a bluish-violet color. In some cases, 
for reasons which we do not know, the amyloid substance does not show a well- 
marked reaction with metliyl violet. Other anilin dyes also differentiate amyloid 
substance from normal tissues. On treating sections of amyloid tissue with solution 
of iodine the degenerated parts acquire a mahogany color. If they are then treated 
with sulphuric acid the degenerated portions acquire a greenish or blue color ; but 
the latter reaction is not very reliable. 




Fig, 8.— Amyloid (Waxy) Degeneration op Capillaries of a Glomerulus in the Kidnby. 
A, waxy capillaries stained with methyl violet; B, normal capillaries. 

Corpora Amylacea are small, spheroidal, homogeneous or lam- 
ellated bodies, which assume a bluish color on treatment with soluticni 
of iodine or iodine and sulphuric acid. They are f recpieiitly found 
in the acini of the prostate gland, sometimes in large numbers ; iu 
the ependyma of the ventricles of the brain, and in areas of sclerosis 
of the brain and cord ; also in extravasations of blood and in various 
other situations. They may occur under normal as well as pjitho- 
logical conditions, and are apparently of little importance. They 
seem to have nothing to do with amyloid degeneration, altlunigh they 
somewhat resemble its products. Some of the tube casts of tlie kid- 
ney resemble in many respects the corp(n*a aiuylacea. 
6 



83 



DEGEXERATIYE CHANGES IN THE TISSUES. 



Glycogen Degeneration. — Glycogen appears under abnormal con- 
ditions in the body as hyalin, mostly globular masses of varying 
size. It is soluble in water, is stained brownish-red by iodine, and 
does not assume a greenish color by the further addition of sulphuric 
acid. In diabetes it may occur in large quantities in the liver cells 
and in the epithelial cells of the uriniferous tubules, especially in 
those of Henle's loop. It may be found in fresh pus cells and in the 
■cells of various forms of tumors. ' 




Fig. 9.— Corpora amylacea. 
From prostate gland. 

Mucous Degeneration may occur in cells or in intercellular sub- 
stance. When occurring in cells it consists, under pathological as 
under normal conditions, of the transformation of the protoplasm into 
a translucent, semi-fluid material, occup}4ng more space than the 
unaltered protoplasm, and hence causing a swelling of the cells (Fig. 





Fig. 10.— Mucous Degeneration of Epithelial Cells. 
From cyst adenoma of ovary. 

10). This ne^j^-formed material contains mucin in solution, which is 
precipitated by acetic acid. It occurs under a variety of conditions, 
sometimes as a morbid increase of a normal function of cells, as in 
many catarrhs, sometimes as an entirely abnormal transformation. 

' If the tissue to be examined for glycogen be fresh the iodine should be used in 
solution in glycerin (equal parts of Lugol's solution and glycerin), in order to avoid 
its solution. Specimens hardened in alcohol are stained with a dilute solution of 
iodine in alcohol (tincture iodine 1 part, absolute alcohol 4 parts), cleared up and 
studied in oil of origanum. 



DEGENERATIVE CHANGES IN THE TISSUES. 



83 



The cells may be entirely destroyed by the accumulation of the mucoid 
material within them. 












f \t 



/': ^^/ 1 






i|7X 



if^f 







fTuJliexv 



Fig. 11.— Mucous Degeneration op Fibrous Tissue of Mamma. 

In certain cases, as in many tumors, in cartilage, bone, and other 
tissues, the intercellular substance undergoes conversion into mucin- 
containing material, losing almost entirely its original structure (Fig. 
11). The cells in such cases may be affected only secondarily by the 
pressure which the new-formed material exerts upon them. 








'^•is^s^^- 






.>5»i 



.tic- 






m 



^^jf>; ■■_■ 















^^^ 



-!.<r,; 



*"/ 



Fig. 13.— Colloid Degkneration op Epithklial Cells* 
From carcinoma of rectum. 

Colloid Degeneration is very closely allied, both in chemical and 
morphological characters, to mucous degeneration, and in many cases 
there is no di^iinite microscopical distinction between them, l^ut col- 



84 



DEGENERATIVE CHANGES IN THE TISSUES. 



loid material is firmer and more consistent than mucous, does not yield 
a precipitate on addition of acetic acid, and its formation is usually 
confined to cells ; not involving intercellular substance, except by an 
atrophy which its accumulation sometimes induces. The cells may 
contain larger and smaller droplets of colloid material (Fig. 12), or it 
may nearly or entirely replace the protoplasm and accumulate to 
such an extent as to cause rupture and destruction of the cell. In 
this way, and by the atrophy of intercellular substance which its ac- 
cumulation causes, cysts may be formed containing colloid material 
and cell detritus. Colloid degeneration is of frequent occurrence in 
certain tumors and in the thyroid gland, and occurs occasionally in 
other places. 

Hyalin Degeneration is the transformation of tissues into a 
transparent, glassy substance, much resembling amyloid in its mor- 
phological characters (Fig. 13) ; but it does not give the micro-chemi- 




Fig. 13.— Hyalin Degeneration of Capillary Blood Vessels. 
From a sarcoma of the optic nerve. 

cal reactions of amyloid, and appears under different conditions. Hy- 
ahn substance is quite resistant to the action of acids and stains 
readily with acid f uchsin and eosin. It occurs especially in the walls 
of the smaller blood vessels in various parts of the body, in voluntary 
muscle fibres, and is said to sometimes involve interstitial tissue. It 
has been described as occurring in the brain, lymph nodes, and ova- 
ries ; in the tubules of the kidney, in the walls of aneurisms, in mus- 
cle fibres, in the lesions of diphtheritis, tuberculosis, and syphilis, in 
the hyaloid membrane and vessels of the eye, and elsewhere. It is 
sometimes called vitreous or fibrinous, and also waxy, degeneration. 
It is believed by some observers that fibrin, blood plates, and leuco- 
cytes may undergo hyalin degeneration. It seems to be, in some 
ways, allied to coagulation necrosis, but its exact significance and re- 
lations to other forms of degeneration, and the conditions of its oc- 
currence, are not yet known. 



DEGENERATIVE CHANGES IN THE TISSUES. 85 

In Calcareous Degeneration there is a deposition, either in cells 
or in the intercellular substance, of larger and smaller granules com- 
posed chiefly of phosphate and carbonate of calcium. These parti- 
cles, when abundant, give hardness, brittleness, and a whitish ajr 
pearance to the affected tissue. Under the microscope they appear 
dark by transmitted, white and glistening by reflected, light. The 
addition of strong acids causes their solution, usually with the forma- 
tion of bubbles of carbonic acid gas, whose evolution may be observed 
under the microscope. Tissues may be nearly completely permeated 
with the salts, or the latter may be scattered in patches through them. 
Sometimes large lamellated concretions are formed in tissues, usu- 
ally at the seat of some old inflammatory process. Calcification usu- 
ally occurs in parts of tissues which are dead or are in a condition oi 
reduced vitality as a result of some antecedent morbid process, usu- 







Fig. 14.— Pigmentation of Connective-tissue Cells of the Lungs. 
From inhaled coal dust— anthracosis. 

ally of an inflammatory nature. Among the most common and im- 
portant examples of calcareous degenerations ma}^ be mentioned those 
which occur in the valves of the heart and walls of the blood vessels. 
Pigmentation. — The pigment which is present in the body under 
abnormal conditions may be formed in the body or may be intro- 
duced into it from without. It may be deposited in the cells or in the 
intercellular substance, and is sometimes visible to the naked eye and 
sometimes not. The pigment occurring in the body may be in the 
form of yellow, brown, black, or reddish granules or in crystalline 
form. In the majority of cases it is formed by the decomposition 
of liiTemoglobin from extra vasated masses of red blood cells. Parts 
which have been the seat of long-continued hypera^mia may hrvve 
a diffuse grayish appearance from the alteration of the haemoglobin 
in red bl(K)d cells which have escaped fn^m the vessels by dia- 
pedesis. Pigment may be formed in the blood vessels in severe cases 
7 



S6 DEGENERATIVE CHANGES IX THE TISSUES. 

of malarial infection, and circulate in the blood. In another class of 
cases various forms of cells seem to be actively' concerned in elabo- 
rating pigment ; this is exemplified in the true melanotic tumors, and 
the process has its physiological prototype in the formation of pig- 
ment in the choroid, skin, and some connective tissues. Pigmenta- 
tion of tissue from the bile occurs under a variety of conditions, and 
may be the result of the deposition of granules or crystals. A diffuse 
staining also frequently occurs from the bile ^vithout the formation 
of solid particles. 

In many cases the mode of formation of pigment is not at all 
understood. In tissues which are normally somewhat colored the 
color may greatly deepen by a simple atrophy of the tissue without 
the new formation of pigment, as in simple atrophy of the heart 
muscle and in atrophied fat. 

As examples of pigment introduced into the body from without, 
we may mention the deposition of minute particles of silver from the 
internal use of silver nitrate ; the coloring of the skin and lymph 
glands from tattooing ; and especially the pigmentation of the lungs 
and bronchial glands from the inhalation of coal and other dust, 
which is universally present under the conditions which modern 
ci^alization imposes. ^ 



^ For the literature on the subjects treated of in this chapter see the extensive 
bibliography in Recklinghausen'' s " Handbuch der allgemeinen Pathologic," which 
constitutes parts 2 and 3 of Billroth and Luecke's " Deutsche Chirurgie/' 1883. 



USTFLAMMATIOS". 



Under the name inflammation is grouped a large and important 
series of morbid processes, in which either various cells of the body 
or the blood vessels, or both, are primarily involved. The inflam- 
matory process embraces widely differing phenomena and brings 
about the most varied structural changes. Owing to its great com- 
plexity and to the diversity of structures which may be concerned, it 
seems to us wise not to try to give a comprehensive definition of in- 
flammation, but, for the purposes of practical study, to group its 
different manifestations into a series of classes or phases, each one of 
which is characterized by the predominance of certain forras of 
structural change or lesion, and to briefly describe these. It must be 
understood, however, that these different classes of inflammation 
frequently merge into one another or are intimately associated, and 
in some cases represent only different stages of the same process. 

ACUTE DEGENERATION. 

{Crranular Degeneration; Cloudy SiveUing ; Parenchymatous 

Degeneration.) 

Under the influence of certain mineral poisons, such as phosphorus, 
arsenic, and mercury, and of a large group of organic poisons de- 
veloped in the body in the acute infectious diseases by the growth 
of bacteria, the parenchyma cells of the viscera, not infrequently 
the heart muscle, and sometimes coiinective tissue, and endothelial 
cells, are apt to swell and become more coarsely granular than 
normal. These new-formed, albuminous granules seem to be de- 
veloped from the protoplasm of the affected cells. When the change 
is moderate in degree the cells may appear simply swollen, and may. 
if the poison ceases to act, return to their normal condition ; or the 
change may be progressive, leading to fatty degeneration of the pro- 
toplasm or to the total destruction of the cell. 

This form of cell degeneration may, and often does, occur without 
other marked lesions (see page 77) ; but as it so freiiuently accom- 
panies various phases of inflammation, and, in its acute form, is so 



88 INFLAMMATION. 

commonly dependent upon the same causes, it may properly be con- 
sidered as forming one of the subsidiary phases of inflammation. It 
must always be taken account of in considering the alterations in 
structure and function which accompany the inflammatory process. 

EXUDATIVE INFLAMMATION. 

In one of the most frequent as well as complex varieties of in- 
flammation the blood vessels play a dominant part ; and as the most 
marked result of the vascular changes is the apj)earance in the tissues 
of certain nevr materials, called exudations, we most frequently speak 
of this variety of inflanmiation as exudative inflammation. 

Xot infrequently at the beginning of an exudative inflammation, 
or when the vascular changes are at no time marked or even at all 
evident after death, the only lesion we find is swelling and turbidity 
and proliferation of the cells of the connective tissue. On free sur- 
faces, such as the peritoneum, pia mater, etc., the swollen and pro- 
liferating ceUs may become loosened and hang off by a pedicle, or 
may collect in groups, or be wdiolly cast off. These comparatively 
few exfohated and new-formed cells under these conditions form the 
entire exudate. 

The most characteristic and common of the exudations are, how- 
ever, semun, fibrin, and p?^5. In order to understand the way in 
which these are produced and the varied post-mortem ajDpearances to 
which their presence gives rise, it is well at the outset to study some 
variety of exudative inflammation in actual occurrence in a li^'ing 
animal. The frog is the most convenient animal for this pui'pose. ^ 

If we expose the mesentery or bladder of the frog so that we can 
study it under the microscope, marked inflammatory changes soon 
occur without other inciting agency than is furnished by the changed 
position and exposure to the air. At first the arteries, veins, and 
capillaries dilate, and the blood, encountering less resistance from 
the walls, flows more rapidly through them. This mcreased rapidity 
of the blood current does not, however, last long, although the ves- 
sels still remain dilated. After a variable period, owing, it is be- 
lieved, to changes of the inner surface of the vessels, the blood meets 
Avith so much resistance that it now flows more slowly than under 
normal conditions. Temporary or even permanent stasis may occur 
in some of the vessels, but this is not a constant nor characteristic 
occurrence. White blood cells — leucocj'tes — now begin to accumu- 
late along the inner walls of the veins and to become fixed there, so 
that after a time the whole inner surface of the veins may be more 

^ That essentially the same phenomena occur in the warm-blooded animals as in 
the frog has been shown by the studies of Thoma and others. 



INFLAMMATION. 



89 



or less thickly sprinkled, and even closely crowded, with adherent 
leucocytes. These may either lie firmly against the endothelium or 
be dragged slowly along by the current of blood sweeping past them. 
Some are dragged by the blood current into pyriform shapes, show- 
ing that they are adherent only at a small point, and thus they may 
be detached from the wall and rejoin the circulating blood. In the 
capillaries, also, leucocytes may be seen clinging firmly to the wall. 
After a tiine, which varies considerably — in the bladder some- 
times within an hour after its exposure ; in the mesentery usually 
much later — some of the leucocytes commence to make their way 
slowly through the walls of the veins and capillaries. At first a little 
shining knob appears on the outside of the wall opposite to the cell 




Fig. 15— Emigration of White Blood Cells ix Inflamed Bladder of Frog. 

which is sticking within, and this outer portion grows larger and 
larger as the part still within grows smaller, until at length the en- 
tire cell is outside of the vessel. The cell now may immediately de- 
tach itself and wander off in the lymph spaces, or it may remain for 
some time attached to the outside of the wall. This passage of the 
leucocytes through the walls of the capillaries and veins — it does not 
occur in the arteries — is called enn'grafioii. The emigrating colls 
are, largely at least, the poly nuclear leucocytes (see page Go). 

The cells pass between the endothelium through the cement sub- 
stance, which becomes in some way changed in the intlammatory 
process. They may pass through very rapidly, but usually their 
progress is slow and often interrupted, so that cells 'may be seen 



90 INFLAMMATION. 

motionless for a long time in various stages of progress through the 
walls. A half -minute, or even less, may suffice for their passage, 
or they may be hours about it. Thus, after a variable time, if the 
conditions have been favorable, the tissues immediately around the 
capillaries and veins, and even those somewhat remote from them, 
may be more or less densely crowded with leucocytes, some motion- 
less and in the spheroidal form, others moving about through the 
Ij^mph spaces. Leucocytes may pass out of the tissues on to free 
surfaces of the inflamed part. 

It is probable that the emigration of the leucocytes is due in part 
to a sort of filtration process with which the pressure of the blood 
within the vessels is concerned. But the inherent contractility of 
the cells themselves forms, doubtless, a very important factor. 

While this is going on the red blood cells, although for the most 
part carried in the usual way along in the axial current of the veins 
and through the capillaries, still usually find their way, in small, but 
sometimes in very large numbers, through the walls of the veins and 
capillaries into the surrounding tissues. They are, it is believed, 
carried passively through the cement substance between the endo- 
thelium by currents of fluid which under these conditions are flow- 
ing in abnormal quantities through the walls. This extravasation 
of the red blood cells is called diapedesis. 

By this time it will usually be found that the tissue around the 
vessels is somewhat swollen and more succulent than normal, and 
fluid may be poured out on the free surface. 

The fluid which is thus formed is called serum, and it is some- 
what similar to simple non-inflammatory transudation, except that it 
contains more albumin and is mixed with cells. This serum has evi- 
dently passed out of the blood vessels along with the blood cells, and, 
as its composition differs somewhat from that of blood plasma, it is 
evident that it has undergone some sort of change as it passed 
through the cement substance of the endothelium. The way in 
which this alteration in the composition of the blood plasma occurs 
as it passes through the walls of the vessels and becomes the serum 
of exudation, we do not understand. 

The fluid exudate contains fibrinogenous substance, and from 
this, when the conditions are favorable, fibrin may be formed by a 
change similar to that which occurs in the coagulation of the blood. 

Thus in the living animal we can learn by direct observation 
the way in which serum, fibrin, and cells get into the tissues and 
upon free surfaces in inflammation. The fate of these exudations 
will be considered further on. 

Under certain conditions diapedesis occurs so extensively that the 
extravasated red blood cells form a very important j^art of the exu- 



INFLAMMATION. 91 

dation, and when this occurs it constitutes the hcsmorrhagic variety 
of exudative inflammation. 

Under varying conditions, furthermore, which depend partly 
upon the seat of inflammation, partly upon its intensity, but of tener 
upon conditions which we do not understand, sometimes one, some- 
times another of the exuded materials preponderate, and we may 
thus have varieties of exudative inflammation which we call mucous, 
serous, purulent, or fibrinous ; or we may have various combina- 
tions of these. 

If the inflammation occurs in a mucous membrane (catarrh) there 
may be at first diminished and afterward an increased production of 
mucus by the mucous cells or glands, which may be so abundant as 
to constitute a variety called mucous exudative inflammation. 

The fibrin, in the fibrinous phase of inflammation, may form in 
the interstices of the tissues, or it may coagulate in membranous 
layers upon free surfaces either in granular or fibrillar form, or both. 
These membranes are called false membranes, in distinction from 
new membranes formed, as will be seen presently, of organized tis- 
sue. In the meshes of the fibrin there may be much or little serum 
and variable quantities of white and red blood cells. The fibrin 
may be stained, by Weigert's method (page 132), of a bluish- violet 
color. 

When large numbers of new cells appear in the exudation col- 
lecting in the tissues or being cast off on free surfaces, we have 
a phase of inflammation called purulent or suppurative inflam- 
mation. 

Hand-in-hand with these changes, which are directly dependent 
upon disturbances of the circulation and alterations of the walls of 
the vessels, there are changes in the connective-tissue cells and 
parenchyma cells of the inflamed region. These changes may be 
degenerative, leading to the death, destruction, and absorption of 
the cells ; or proliferative, leading to the formation of new cells. 
The new cells may resemble the ariginal cells of the part, or the emi- 
grated leucocytes or their progeny. 

We have seen that an excessive accumulation of fibrin in the tis- 
sue in exudative inflammation may cause death of a circiunscribed 
portion of it. Death of tissue in inflammation may be caused in 
other ways, as by permanent stasis in the blood vessels, by the local 
action of bacteria, etc. ; and as this death of tissue, which may either 
cause the inflammation or be secondary to it, forms a prominent fea- 
ture in the process, we speak of it as necrotic iiiflamiU((fioN. 

Again, there may be in inflammation a. disintegration and break- 
ing-down of tissues, either associated with cu- determined by accumu- 
lations of pus cells within them. This is called /Hflanntnifioii in'fh 



92 INFLAMMATION. 

formation of abscess, and may be acute or chronic and arise from 
a variety of causes. 

On free surfaces death of superficial areas of tissue, giving rise to 
ulcers, may be simply associated with or dependent upon the inflam- 
matory process. This we may call ulcerative inflammation. But 
in these, as in many other subordinate varieties of inflammation, 
which it is not necessary to describe here, the fundamental processes 
are, it should be remembered, essentially the same. 

Suppurative inflammation is, in the majority of cases, due to 
the presence and growth of bacteria in the body. These may act 
largely by stimulating the emigration of leucocytes, or, in addition 
to this effect, they may cause cell proliferation or necrosis of tissue 
(see page 76). Suppurative inflammation may be incited by vari- 
ous chemical substances, such as calomel, turpentine, etc. But this 
form of non-bacterial suppuration is not of that active, progressive 
charaeter which self -propagating agents like bacteria may induce. 

We have now to consider what becomes of these exudations 
and the degenerated and proliferated cells. Mucus usually passes 
off on the surface with other exuded materials, but may collect in 
considerable quantities in the cells in which it is forraed or in the 
acini and ducts of the mucous glands. The extravasated red blood 
cells lose their hsemoglobin, which decomposes and may be absorbed 
or deposited as granules or crystals in the tissues, while the cells 
themselves disintegrate and are absorbed. The serum may pass 
off on free exposed surfaces, or in a short time be taken again 
into the circulation by means of the lymph channels; or it may accu- 
mulate in serous ca\dties, where it may remain for a long time, 
mingled mth other exudations. The fibrin may form in such dense 
masses in the interstices of the tissues as to interfere with their nutri- 
tion, and thus circumscribed portions of tissue may die and be ab- 
sorbed or thrown off as sloughs with their contained fibrin. Fibrin 
may disintegrate and be finally entirely absorbed, it may be thrown 
off on exposed surfaces, or it may be gradually replaced by a new- 
formed vascular organized membrane or mass of tissue, the ab- 
sorption of the fibrin going on hand-in-hand with the formation of 
the new tissue. 

The fate of the leucocytes varies greatly and is in many respects 
still obscure. A certain number of them, after leaving the blood 
vessels, wander through the tissues, and, entering the larger lymph 
vessels, again join the circulating blood. Others, there is reason to 
believe, undergo proliferation and thus add to the number of the 
infiltrating cells. Still other leucocytes die, either in the interstices 
of the tissues or after passing off on free surfaces; they may then 
disintegrate and be absorbed, or they may collect in masses wdth 



INFLAMMATION. 



9:3 



other exudations in internal cavities, or they may collect in circum- 
scribed masses in the interstices of the tissues, and, in connec- 
tion with other cells and more or less fluid and broken-down tissue, 
form abscesses. 

The term pus is rather loosely and indiscriminately applied to the 













Tig. 16.— Pus Cells from Catarrhal Inflammation of Bronchial Mucous Membrane. 

new cells which we find in the tissues in exudative inflammation, 
when these are not actually concerned in the formation of new tis- 
sue. It would be better to speak of these new cells, whose morpho- 







Fig. 17.— Omentum of Dog, showing Peritonitis on Fourth Day, x 5(X) and reduced. 



logical characters give us no clue to their destinies, as in(Jiffe)'ent 
cells, and limit the term pus cells to those cells which, prculucotl in 
inflammation, have evidently died in or about the tissue, and which 
we call, in the surgical sense, pus. 

Since the great majority of nmv colls s hmi iu acute cxudativt^ 



94 INFLAMMATION. 

inflammation are in fact extra vasated leucocytes or their progeny, 
the appearances of the ordinary pus cells are essentially the same as 
those of the leucocytes, except that they may exhibit degenerative 
changes. Thus they may present various degrees of fatty degenera- 
tion and disintegration, and the nucleus is frequently broken into 
fragments, thus simulating the commencement of proliferative 
changes. 

In exudative inflammation of the serous and mucous membranes 
we often find, in addition to the ordinary pus cells, larger and vari- 
ously shaped cells, which are detached epithelial or endothelial cells 
(Fig. 17) or the result of their proliferation. These, although usually 
present in relatively small numbers, must still be considered pus 
cells in accordance with the views above laid down. Moreover, we 
must remember that the fixed connective-tissue cells, as well as en- 
dothelium and epithelium, may give rise by proliferation to cells 
which we cannot distinguish morphologically from the emigrated 
leucocytes. 

EXUDATIVE INFLAMMATION WITH PRODUCTION OF NEW TISSUE. 

{Reparative Inflammation. ) 

In many cases of exudative inflammation, after the subsidence of 
the active changes in the blood vessels, the exudations are entirely 
absorbed and the tissue returns to its normal condition ; this we call 
resolution. Under certain conditions, on the other hand — for ex- 
ample, in the case of a wound with loss of substance, or in an acute 
exudative inflammation of a serous membrane where the surface is 
deprived of its normal endothelial covering, or in the healing of an 
abscess — new tissues may be formed through the agency of the new 
cells produced in the inflammatory process. 

Such inflammation with the formation of new tissue is sometimes 
called reparative inflammation, and the new tissue may be conser- 
vative and of value to the organism, as when it fills up a wound ; or 
it may be very detrimental when tissues are formed where they do 
not belong. 

Healing of Wounds. — The way in which new inflammatory tis- 
sues are formed may be best understood by following the process of 
healing in a wound with loss of substance — say, for example, a 
wound through the skin into the tissues beneath. At first there 
may be hsemorrhage. After this has ceased, the injury to the tissue, 
the unusual exposure of deep-seated parts, the presence of foreign 
substances, etc., may induce the same series of events which we 
have seen occurring in exudative inflammation with production of 
serum, fibrin, and pus. The blood vessels dilate, the circulation 



INFLAMMATION. 95 

becomes slower, serum transudes, and emigration sets in. Certain 
of the cells and fragments of intercellular substance near the seat 
of injury may die and in time are cast off or absorbed, the tissue 
becomes soaked and swollen by the transuded serum, and the con- 
nective-tissue cells in the vicinity may undergo proliferative or de- 
generative changes. 

After a variable time, usually on the second or third day if all 
goes well, the surfaces of the wound may be more or less covered 
with tiny red nodules called granulations. These granulations con- 
tain numerous thin- walled blood vessels which have sprouted out 
from the old vessels near the seat of injury, and around these a new 
loose, succulent tissue is formed, largely, if not wholly, it is believed, 
from proliferation of connective-tissue cells. On the surfaces of the 
granulations are usually a greater or less number of pus cells. 




\^ hOL' 






Fig. 18.— Developing Blood Vessels in New-formed Tissue. 

In the formation of new blood vessels in granulation tissue there 
are at first delicate sprouts of solid protoplasm, from the cells of the 
wall of the original vessels of the part or from those which have been 
newly formed, reaching out among the exudation cells. These 
sprouts may extend for long distances and may form anastomoses 
with similar sprouts from the same or other vessels (Fig. 18). They 
consist at first of solid protoplasm, and become gradually channelled 
out by the pressure of the blood in the vessels from which they 
spring ; the blood finally entering them and forcing its way along 
them, producing a lumen as it goes. Before this channelling of the 
lumen, and hand-in-hand with its progress, new nuclei are formed in 
the protoplasm and the new-formed walls gradually assume a distinct- 
ly cellular character. At length they have well-di^tiiuMl endothelial 
walls, cells from without range themselves along o\itside o{ them, 
and they take their place in the vascular system of tlu^ utnv tissue. 



96 



INFLAMIVIATIOX. 



Thus, in a very short time, multitudes of new blood vessels may 
form, furnishing nutritive centres around which the organization 
of tissue proceeds. 

The cells of the granulation tissue are at first mostly small and 
spheroidal, and are usually packed pretty closely together with only a 
small amount of fluid intercellular substance. Presently some of 
the cells become larger, elongated, fusiform, or branched, and after 
a while a delicate, fibrillar intercellular substance makes its appear- 
ance about them and grows more and more abundant (Fig. 19). 




^#-^ X 






\L 







Fig. 19.— Granulation Tissue from Wound of Skin. 



These larger, variously shaped cells, which appear to be formed out 
of the small spheroidal or indifferent cells of the granulation tissue, 
are usually granular, and the nucleus is usually large and distinct, 
frequently exhibiting a well-marked intranuclear network. Since, in 
some respects, these cells when first formed resemble some kinds of 
epithelial cells, they are often called the epithelioid cells of granula- 
tion tissue. Some of these larger cells seem to be more or less direct- 
ly concerned in the formation of intercellular fibres. These appear 
to develop either as filamentous branches of the cells or to be formed 
along their sides. Such fibre-forming cells are called fibroblasts 
(Fig. 20).^ 

All this time new small spheroidal indifferent cells are gathering, 
by proliferation or by continued emigration. Some of these seem to 
participate in the formation of the granulation tissue, while others, 
not finding conditions suitable for their further development, or even 
for their continued existence, die and pass off on the surface, together 



INFLAMMATION. 



97 



with some transuded fluid, as pus. The new tissue gradually be- 
comes more and more dense, the intercellular substance more abun- 
dant, while the cells decrease in number and become flatter and less 
conspicuous. The epithelium may now grow over from the sides and 
cover the new tissue. The new tissue, having at last undergone 
more or less shrinkage, consists of a dense, firm mass composed 
largely of fibrillar basement substance with a few flattened cells 



./ ,^ 



r> 









/> 

■" y ' 



//*-' 






^ . . . 



, / ^ y 



"y 



/^ 






^ /' ^ . 






yy<-{i 



/ 
V 









yy". 

y 



^Y^^ ^' 



y 



^.■^' 



Fig. 20.— Fibroblasts from Granulation Tissue, 

(Fig. 21); and with this, which is the cicatrix^ the healing is com- 
plete. 

Although in the production of new tissue in connection with or 
following exudative inflammation essentially the same processes are 
involved in all cases, there are yet very marked differences in the 







Fig. 21.— Cicatricial Tissue. 



degree in which the different factors share. Thus the vascular and 
exudative phenomena may predominate and very large quantities of 
serum, fibrin, or pus be f(n*med, while the amount of new-formed tis- 
sue may be very insignificant. In other cases the formation of new 
tissue is the dominant feature in the process, and the production of 
exudations seems to be almost entirely subordinated to this end. 
The distinction between healing bv the first and second intention. 



98 INFLAMMATION. 

which is of practical importance in surgery, is. from the pathologi- 
cal standpoint, only a quantitative one. For the restitution of the 
parts to the healthy condition is in both cases brought about by exu- 
dation, and proliferation of cells under the influence of vascular 
changes ; but in one case the latter changes are very slight, in the 
other more or less extensive. 

A good deal of variation is frequently seen in the formation of 
granulation tissue in the healing of wounds, as well as under other 
conditions. Thus sometimes the body cells respond but imperfectly 
to the inflammatory stimuli, and neither cell proliferation nor blood- 
A^essel growth is active. On the other hand, the development of 
blood vessels may be excessive, other tissue formation lagging behind. 
Under these conditions loops and tangles of thin- walled, contorted 
new vessels may project from the granulating surface, while useful 
tissue formation remains in abeyance (Fig. 22). The result of this 



/-^ 




Fig. 22.— Exuberant Granulations- 
From the inner surface of a granulating ovarian cyst containing pus. 

disproportionate growth of ill-formed blood vessels is the exuberant 
granulations which the surgeon frequently removes from unhealthy 
healing surfaces. 

Abscess ca^dties in any part of the body may be filled up and 
their sides drawn together in a cicatrix by the formation of a pro- 
visional mass of granulation tissue similar in character to that which 
grows in external wounds. So, similarly, cysts may be obhterated 
and ulcers partially filled and drawn into cicatricial healing. Large 
free surfaces, like the pleura and peritoneum, may, through the in- 
tervention of granulation tissue, pass from the denuded condition 
of a active exudative inflammation, either with or without adhesions, 
into a condition which, though by no means a return to the normal, 
we yet designate as cure. 

Healing of Bone Fractures.— The process of heahng in bone 



INFLAMMATION. 99 

after fracture is, when uncomplicated, at first similar to that in ordi- 
nary healing by second intention in fibrous tissue. The blood and 
other exudates and the tissue detritus are gradually absorbed or dis- 
posed of by phagocytes/ By a proliferation of connective-tissue 
cells of the region a larger or smaller mass of granulation tissue is 
formed. This granulation tissue does not at first differ in appear- 
ance from similar tissue formed elsewhere in the body in the repara- 
tive phase of exudative inflammation. 

But soon, under the influence of the specially endowed cells of 



cH ^>- ■_. . - 



^-^j - ^ ^r ^fk 












d) ^ 













Fig. 23.— New-formed Cartilagk and Osteoid Tissue from Callus after Fracture of the 

Femur. 

cartilage or bone or periosteum, but especially of the latter, the 
granulation tissue becomes partially replaced either by cartilage, or 

' The disposal of small foreign particles which in one way or another get into the 
body, and the removal of dead and useless fragments of tissue which may be present 
as the result of injury or disease, are cared for by larger and smaller cells, called 
phagocytes. The cells having this matter in charge are largely leucocytes, and all are 
apparently mesodermal lowly organized cells. Some of them are large cells and may 
be multinuclear. The disposal of dead or foreign material is accomplished primarily 
by being taken into the bodies of the phagocytes. These may either retain it more 
or less permanently, or may absorb it in virtue of their metabolic powers, or may carry 
it off to some region of deposit by the exercise of their amivboid capacities. This 
phagocytic action of mesodermal cells is believed by some observers to have an im- 
portant bearing upon immunity from, and cure of, bacterial disease (see page 100^. 



100 INFLAMMATION. 

by a substance resembling bone in general appearance, but contain- 
ing no lime salts. This is called osteoid tissue. These new carti- 
laginous and osteoid tissues, which are apt to occur together, form 
irregular masses or interlacing trabeculse in the stroma of granula- 
tion tissue.. This constitutes the so-called callus of a uniting frac- 
ture (Fig. 23). 

Gradually, however, the osteoid tissue becomes osseous, and 
the masses of cartilage and bands of periosteal and other fibrous tis- 
sue, under transformations practically identical with those seen in 
normal development, are converted into bone. Thus by gradual ab- 
sorption and reformation of bone in the usually redundant provisional 
bony mass, and the readjustment of its vascular channels, the heal- 
ing, with more or less permanent deformity, is accomplished. 

CROUPOUS INFLAMMATION. 

This form of inflammation, which usually occurs on mucous 
membranes, is characterized by the formation of fibrinous material 
either upon the surface or infiltrating more or less deeply into the 
tissue. This layer of new material is called a false membrane, or 
jjseudo-membrane, and, in addition to fibrinous material, may con- 
tain pus cells in various stag^es of degeneration, desquamated epi- 
thelium, and various forms of bacteria. The false membrane may 
be quite thick, or so ,thin as to be almost invisible. The fibrinous 
material may be present in the form of well-defined fibrils, or in the 
form of granules, or as irregular amorphous masses. It may be 
formed by the coagulation of fluids exuded from the blood vessels, or 
by transformations of the epithelial cells by coagulation necrosis, and 
these may then present various irregular branching forms. The 
mucous membrane under these conditions usually exhibits the lesions 
of an acute catarrhal inflammation. 

Owing to the dense infiltration of the mucosa with fibrin or other 
products of inflammation which sometimes occurs, or from other 
causes, circumscribed portions of tissue may die and be cast off, 
giving rise to ulceration. 

Pseudo-membranous inflammation may occur on the surface of 
wounds, or even on the skin, and may be caused by a variety of agen- 
cies. It may be due to severe heat, as from steam. Strong acrid 
vapors, such as those of the mineral acids, may induce it. In its 
most common and significant form it is due primarily to the pre- 
sence in the affected regions of pathogenic micro-organisms. One of 
the most serious forms of croupous inflammation is caused by the 
presence at the seat of lesion of the Bacillus diphtherise of Loffler, 
and, forming then a part of a general disease, it is called diphtheritic 
inflammation, (See Diphtheria, page 198.) Very frequently a 



INFLAMMATION. 



101 



pseudo-menibranous inflammation of the mucous membrane occurs, 
similar in its morphological characters to diphtheritic inflammation, 
but caused by the presence and action of a streptococcus. This form 
of inflammation, which is of frequent occurrence in connection with 
scarlet fever and measles, but which may occur by itself, is called 
simple croupous inflammation, ov pseudo-diphtheritic inflamma- 
tion (see page 160). 

Some observers, it should be said, attempt to make a morpho- 
logical distinction between croupous and diphtheritic false mem- 
branes, calling those cases croupous in which the false membrane 




Fig. 24.— Croupous Inflammation op Trachea. 
In this case there is purulent infiltration of the mucosa and submucosa, and of portions of the 
mucous glands, a, false membrane ; 6, portion of intact epithelium ; c, infiltration of the mucosa 
with fibrin ; d, portion of mucous gland infiltrated with pus. 



does not infiltrate beneath the epithelium ; diphtheritic, those in 
which the infiltration extends into the mucosa beneath the epithelium 
and the basal membrane. This distinction does not, as above stated, 
seem to us justified by the facts ; the essential difference between 
croupous and diphtheritic inflammation being primarily an etiologi- 
cal one, depending, in the infectious forms of the disease, upon the 
species of pathogenic micro-organisms which cause the lesion. 

PRODUCTIVE INFLAMMATION. 

(Hyperplastic or Interstitial luflanuuafiou.) 

Under a variety of conditions, which for the most part we do 
not understand, there is a new production of connective tissue in 

8 



102 INFLAMMATION. 

the body not associated, so far as we know, with marked vascular 
changes such as we have seen in exudative inflammation. We sim- 
ply find, in various parts of the bod}', but particularly in the inter- 
nal organs, an increased amount of connective tissue. In such or- 
gans as have a well-defined separation of structures into parenchyma 
and interstitial tissue, it is the latter tissue which is increased in 
amount (Fig. 244). The new tissue may be moderately rich in cells, 
or it may be dense and have the character of cicatricial tissue. It 
seems, as all pathological new-formed connective tissue does, to un- 
dergo shrinkage as it gets older, and hence the parenchyma cells, 
and consequently the functions of organs, may be greatly interfered 
Avith, and even almost entirely destroyed when it is formed in any 
considerable quantity. Organs which present the earlier stages of 
productive or interstitial inflammation may be larger than normal, 
but in later stages they are almost invariably smaller, and may be 
variously distorted by the shrinkage of the new-formed tissue. 

This process is usually, if not always, a slow or chronic one, al- 
though in most cases we do not know exactly how or when it begins. 

The new tissue formed in typical productive inflammation is prob- 
ably largely developed from the connective-tissue cells of the organ 
involved. In certain cases its formation appears to be secondary to 
degenerative or atrophic changes in the parenchyma cells of the 
part. 

Acute exudative inflammation in any of the tissues or organs may 
give rise, as we have seen, to the formation of new connective tissue; 
but masses of new tissue thus formed differ usually in topographi- 
cal distribution from the more slowly developed interstitial hyper- 
plasias which we are considering. We must, however, admit the 
possibility that some of the cases which seem, when we see the organs, 
to have been simple hyperplasias, may have passed through ante- 
cedent phases akin to, or of real, exudative inflammation. 

SPECIAL FORMS OF INFLAMMATION. 

As the result of the presence and growth in the body of various 
forms of micro-organisms, a series of lesions occur which might he 
appropriately classed as special types of inflammation. These are 
often associated with one or more of the phases of simple inflamma- 
tion which we have just considered. Such special types of inflam- 
mation induced by bacteria, such as tuberculosis, syphilis, pneumo- 
nia, diphtheria, etc., will be described in detail in the section devoted 
to the Infectious Diseases, and in the part of this book in which 
lesions of special organs are described. 



PARASITES. 



The scope of this work permits us to do little more than enumerate 
and give a very brief description of some of the more important 
forms of animal parasites found in man. Among the vegetable 
parasites, however, the bacteria have assumed such an important 
place in our knowledge of the etiology of certain diseases that they 
justly claim a somewhat extended consideration. 




Fig. 25. — Am<eba Coli. 

From the intestinal wall near an ulcer. Drawn from a specimen prepared by Prof. W. T. 
Councilman. 

ANIMAL PARASITES. 
PROTOZOA.' 

Several genera and species of protozoa are found in the human 
body, some of which are of extreme significance. 

The Amoeba coli has been repeatedly found in chronic dysentery 
in the intestinal contents, at the bottom of the intestinal ulcers, and 
in the secondary abscesses, especially of liver, which may accompany 



^ For a resume of our present knowledge of the parasitic protozoa consult Krust\ 
" Der gegeuwilrtige Stand unserer Kentiiisse von don parasitiireu Protozoou," Ily- 
gienisclie Rundschau, ]\Iay and June, 189*3. 



104 PARASITES. 

ulcerative colitis. The amoeba is believed to be the cause of both the 
primary ulcerative colitis and its complicating abscesses (see page 
■i74). 

The Amoeba coli is a single spheroidal cell, from ^Ye to eight 
times the diameter of a red blood cell, with granular protoplasm and 
a vesicular nucleus. It often contains larger and smaller vacuoles. 
Frequently, especially when the amoeba is active, a portion of the 
protoplasm appears almost homogeneous — ectosarc — while the rest — 
endosarc— is granular. When in action, in virtue of the amoeboid 
movement, it may assume various forms, thrusting out and with- 
drawing nearly homogeneous pseudopodia. It may also change its 
shape without progressive movement. It occurs in connection with 
chronic dysentery, frequently in Egypt, occasionally in Russia, and 
a number of cases have been recorded in this country by Councilman ' 
and others. 

Coccidia, — The so-called psoro^permfce — minute oval structures 
about 0.035 mm. long, with a thick capsule and coarsely granular 






Fig. 26.— Coccidium oviforme. 

From liver of rabbit. Showing phases in the development of the psorospermiae, which are 
seen separate within the capsule in C. After Braun. 

contents — which are of very frequent occurrence in the liver of the 
rabbit, forming a part of the contents of yellowish, irregular-shaped 
cysts, have been found in the liver, in a pleuritic exudate, and in the 
kidney, ureter, and heart muscle in man. The organism is more 
properly called Coccidium oviforme (Fig. 26), while the spores which 
it forms are termed psorospermisB. 

Another, smaller form, occurring in the intestinal epithelium of 
dogs, cats, and rabbits, has been found in two cases in a similar 
situation in man. 

Organisms apparently belonging to the coccidia have been found 
in certain contagious epithelial growths — Molluscum contagiosa m 

It is believed by many that Paget's disease and other somewhat 
similar skin affections are due to the presence of coccidia. The claim 
that some of the carcinomata may be caused by coccidia does not 
appear to rest on a substantial basis (see page 230). 

^ We refer for further details concerning the Amoeba coli to the work of Coun- 
cilman and Lafleur on " Amoebic Dysentery," Johns Hopkins Hospital Reports, voL 
ii., Nos. 7. 8. 9, 1891. 



PARASITES. lOo 



The Plasmodium malarice, which is believed to be the primary 
etiological factor in intermittent fever, is described elsewhere (p. 121). 

Among the infusor^ia we find in man representatives of several 
genera. 

Balantidium coli is an ovoidal organism, from 0.06 to 0.1 mm. 







i^ 



■0^-^^^74, 






Fig. 27.— Balantidium Coli. After Braun. 



long, with cilia along the sides, which occurs occasionally in diar- 
xhoeal discharges in northern Europe (Fig. 27). 

Cercomonas intestinalis is a pear-shaped, flagellate structure 
(Fig. 28), about 0.012 mm. long, making, when alive, rapid move- 




FiG. 28.— Cercomonas intestinalis. After Braun. 

ments. It has been found in the evacuations of persons suffering 
from cholera, typhoid fever, and diarrhoea. 

Trichomonas vaginalis has an oval or pear-shaped body, about 
0.01 mm. long, on which are a few cilia, and at the end two or three 
flagella somewhat longer than the body (Fig. 29). They are of very 




Fig. 29.— Trichomonas vaginalis. 



frequent occurrence in acid vaginal exudations in catarrhal vaginitis. 
The possibility of mistaking the T. vaginalis for human spermatozoa 
should be borne in mind in medico-legal examinations, although to 
an observer familiar with either structure such a mistake could 
hardly occur. 

The protozoa may be studied iii the living coudition either in the tiuids in which 
they are found or in three-quarter-per-cent salt solution. They may be killed and 
preserved by allowing a drop of one-per-cent osmic acid to run under the cover glass, 
and replacing this after an hour by glycerin lightly tinged with eosiu. 



106 - PARASITES. 

Many of the smaller forms show well when dried on the cover glass and stained 
by the anilin dyes by the methods used for bacteria (see page 130). 

The movements of the Amoeba coli may be studied on the warm stage in the 
faeces, which frequently contain them in enormous numbers, or in three-quarter-per- 
cent salt solution. Its morphology may be studied in tissue containing them, such 
as intestinal ulcers, abscesses, etc. , which have been hardened in alcohol and stained 
either with methylen blue or hsematoxylin, the former being especially commended 
by Councilman and Lafleur. 

WORMS. 

Trematoda (Flukes). — These worms are small, flat, tongue- 
shaped or leaf -like creatures, with an intestine, and discoidal struc- 
tures on the under surface, by means of which they attach them- 
selves. There are several genera and species found in man. The 
most common genus is Distoma, Of these D. liepaticum is of most 
frequent occurrence (Fig. 30). 

It is about 30 mm. long, and usually occurs in the gall ducts and 
gall bladder. The embryos are attached generally to water plants, 
from eating which the infection is believed to 03cur. D, laiiceola- 




FiG. 30.— DisTOMA HEPATicuM. About natural size. 

funi is more slender, pointed at the ends, 8 to 10 mm. long, and has 
been found a few times in the gall bladder. D, sineuse is a slender 
worm about 15 mm. long, and has been found in the bile in consid- 
erable numbers, particularly in the Chinese. D. hcemafobium is a 
more nearly cylindrical worm ; the sexes are distinct ; the male from 
12 to 14 mm. long, the female 16 to 18 mm. long, and occurs, espe- 
cially in Egyptians, in the portal and other abdominal veins. 

Cestoda (Tape Worms). — These importa;nt worms consist, in the 
mature state, of more or less rectangular or elongated segments, 
each one of which represents a single individual, arranged in a linear 
series to form a colony, at one end of which, called the head, is a 
variously formed structure for the attachment of the colony to its 
host. The neck and head are called the scolex, while the segments 
are called joroglott ides. These worms have neither mouth nor ali- 
mentary canal. They are hermaphrodites, the' sexes being united 
in the proglottides. The head and neck (scolex) may exist as an 
immature form in various tissues and organs where they are en- 
cysted, and are often called cysticercus. 

Tcenia solium is of frequent occurrence in man. It may be 
several metres in length, and may be coiled up or stretched out in 
the small intestines. Several worms may be in the gut at one time» 



PARASITES. 



107 



The head, about the size of a pin's head (Fig. 31), has a projecting 
proboscis or rostellum, around which are arranged a double row of 
horny booklets. Below these are four sucking discs at the sides of 
the head. The booklets of the anterior row are larger than those in 
the posterior row, and are from 0.16 to 0.18 mm. long. The proglot- 
tides, when fully developed, are from 10 to 12 mm. long and from 5 
to 6 mm. wide, but those nearest the head are much shorter and im- 
mature. The eggs of T. solium are ovoidal structures, about 0.03 
mm. in diameter. The embryo of this worm is most commonly seen 
in the muscles of the pig as an encysted scolex, commonly called a 
" measle.^'' It occasionally occurs in man in the muscles, brain, eye. 



W^^ 




■.•■.,i^-'f: ■■;, 













'-. ''.V ' - "■' ; ■' ■■■ '.•■ ■::'■ ■■ v.>.'.'.'V-'-?i^i| 



^■^■-y^^MB^'-. 



v'.v-.^''<-; }■■■ .:-''''y--^ 









Fig. 31. 







■:^^m:m''X 





Fig. 32. 



Fig. 31.— Head of T^nia solium, x about 40. 

Fig. 32.— Head and Proglottides of T^nia mkdiocanellata. 

A, head, x about 15. 

B, mature proglottid, showing generative apparatus. 

C, head and fragments of Immature proglottides, showing gradual tapering of the neck. 
Natural size. 



etc., and is called cijsticercus cellulosce. It is usually about the 
size of a pea, but may be as large as a pigeon s egg and surrounded 
by a connective-tissue capsule. 

Infection with the worm occurs in the human subject from the 
ingestion of insufficiently cooked " measly '' pork, or, in the case of 
cysticercus cellulosse, from the ingestion of the eggs, which may, in 
a variety of ways in uncleanly persons, get into the food. 



lOS 



PARASITES. 



Tcenia mediocanellata {T. saginata Leuckart). — The head of 
this species is somewhat cuboidal. without either rostellum or hook- 
lets, but with four sucking discs (Fig. 32). The segments are gen- 
erally broader and shorter than in T. solium, and the worm is usually 
larger. In the embryonal form the scolex occurs as the Cysticercus 
tcenice mediocaneUafce in the form of small cysts in the muscles of 
cattle, from the eating of which in the uncooked condition the infec- 
tion occurs. This is the most common tapeworm in the United 
States. 

Tcenia ecliinococcus. — This worm in the mature condition 




Fig. 33.— CuncuLA of EcHrxococcrs Cyst. 
Showing lamellated structure. 

forms a short, small colony inhabiting the intestine of the dog. 
The head is about 0.3 nun. in diameter and has a double row of 
booklets around the rostellum. The proglottides are three or four 








Fig. 34. — Scolices of T.esia echetococcus, ;< 60. 
In one the rostellum is projected, in the others it is -nithdrawn. 

in nmnber, the last being the larger. The entire colony is not more 
than -4 to 5 mm. in length. The sigTiificance of this parasite in hu- 
man pathology depends upon the cysts, called hydatids, which it 
forms, in the immature or cysticercus stage, in various parts of the 
body. Intimate association with dogs favors the acquirement of this 



PARASITES. 109 

parasite. When the eggs of the mature worm get into the intestinal 
canal of man they undergo partial development and find their way 
into the tissues and organs, most frequently into the liver. Here 
cysts are formed which become encapsulated by a connective-tissue 
membrane produced by the inflammatory reaction of the organ. 

The cyst wall of the parasite is formed of two layers — an outer, 
finely lamellated layer called the cuticula (Fig. 33), and an inner, 
granular layer, containing muscle fibres and blood vessels, called the 
parenchymatous layer. Inside of the primary cyst secondary cysts 
sometimes form, called daughter cysts, and within the latter tertiary 
cysts, called granddaughter cysts, may develop. On the inner sur- 
face of the cysts, either primary, secondary, or tertiary, the scolices 
or heads of the immature worm are formed. These develop in the 
walls of the pediculated vesicles called brood capsules. The walls 
of these vesicles have a lamellated cuticula and a parenchymatous 
layer similar to those of the primary cysts. The scolices, of which 




Fig. 35.— Hooklets from Scolex of T.^nia echinococcus. 

there may be several in each brood capsule, are similar to the heads 
of the mature tapeworm. They are about 0. 3 mm. in diameter, hav- 
ing a rostellum surrounded by a double row of hooklets and four 
sucking discs. At the posterior end of the scolex is a pedicle by which 
it is originally attached to the wall of the brood capsule (Fig. 34). 
Little, lamellated concretions of lime salts are often present in the sco- 
lex. The anterior portion of the scolex, the rostellum. hooklets, and 
suckers, are often invaginated in the posterior portion. The scolices 
may be free inside of the brood capsules, or, owing to the rupture of 
the latter, they may be free in the cavity of the primary cysts. They 
may die and degenerate, forming a granular mass in which the book- 
lets may be embedded, or the hooklets may be free in the brood cap- 
sules or in the primary cysts. Sterile cysts are often found, that is, 
those in which neither brood capsules nor scolices are developed. 

The cysts contain, in addition to the scolices, a clear, gelatinous 
fluid. This fluid may become turbid by admixture with disinte- 
grated scolices or fragments of the parenchymatous layer, or it may 



110 PARASITES. 

contain fatty detritus, cliolesterin crystals, and particles of lime salts. 
The fluid may be partially a^bsorbed, leaving a thick, grumous mate- 
rial within the cysts, which may become calcified or converted into a 
stony mass. When the scolices are not found entire the diagnosis 
may be made by the discovery of the separate booklets (Fig. 35) or 
fragments of the characteristically lamellated cyst walls. The con- 
nective-tissue walls of the primary cysts may become fatty or cheesy 
or calcified. 

Sometimes the secondary vesicles project outward instead of in- 
ward, forming a series of cysts outside of the primary one. This va- 
riety of development is sometimes seen in man, but is more common 
in the domestic animals. It is called Ecliinoccociis scolecipariens 
or exogena. 

Another variety of echinococcus, called E. multilocularis, is 
almost always found in the liver, and appears to be the result of in- 
complete and disturbed development of the embryos or cysts. It con- 
sists of a congeries of irregular, usually small cysts, surrounded by 
broad and narrow bands of connective tissue, and sometimes contain- 
ing gelatinous fluid and scolices or booklets ; but the latter struc- 
tures are commonlv absent or difficult of detection. The whole is 
often surrounded by a dense connective- tissue capsule which may be 
calcified. The entire mass often presents an alveolar structure and 
was formerly regarded as a tumor — alveolar cancer. The diagnosis 
may be established by the discovery of the booklets or scolices, or 
fragments of the lamellated cuticula (see page 109). 

There are four or five other species of tsenia, occurring rarely in 
man. 

Tcenia nana. — This species occurs in the form of small colonies 
about 15 mm. in length. The rostellmn is surrounded by a single 
row of booklets. It has been seen once in large numbers by Bilharz 
in the duodenum of a child which died of meningitis in Cairo. 

Taenia flavopunctata, a species about which little is known, is 
reported twice in America as occurring in the intestine of young 
children. . 

Taenia madagascariensis, also little known and rare, has been 
seen in two children in Madagascar. 

Tcenia cucumerina. — This species occurs in colonies about 20 
cm. long. The head is very small and spheroidal, and has four rows 
of booklets. It is frequent in the small intestines of dogs or cats. 
It occurs occasionally in man. Its scolex inhabits the dog louse, and 
infection may occur in man by the transference of the lice or the em- 
bryos of the parasite to the mouth, as the result of the filthy habit of 
kissing dogs and cats or permitting the face to be licked by them. 

BotJirioceplialiis latus. — This, the largest of the human tape- 



PARASITES. 



Ill 



worms, has very broad, quadrangular proglottides. The head is 
ovoidal and about 2 mm. long and 1 mm. broad. It has no proper 
sucking discs and no booklets, but by long grooves on either side of 
the head the animal attaches itself to its host. The neck is long and 
filiform. It occurs most frequently in Europe, particularly in the 
northern provinces. The eggs undergo partial development in water, 
and are taken up by the pike and eel-pout, and perhaps by other 
fresh-water fish, from the ingestion of whose flesh in an imperfectly 
cooked condition the human infection occurs. Two other species of 
Bothriocephalus have been described as of rare occurrence in man : 
B, cordatus in Greenland and Iceland, and B. cristatus, 

jSTematoda (Round Worms). — These worms are in general cylin- 
drical, elongated, usually pointed at the ends, and sometimes fili- 
form. The surface is sometimes smooth, sometimes irregularly beset 
with hairs and papillae, or possesses longitudinal elevated striae or 
transverse rings ; but the body is not segmented. There is a mouth 
at the anterior portion, and a ventral anus near the posterior end. 





Fig. 36. — Ascaris lumbricoides. About half natural size. 
A, Ma]e. B, Female. After Perls. 



The intestine is straight. The sexes are in most forms distinct, the 
male being in general smaller than the female. 

Ascaris htmbricoides. — This is one of the most common of the 
human intestinal parasites, and is of particularly frequent occurrence 
in children. It is of a light-brownish or reddish color. The female 
is from 30 to 40 cm. long and from 5 to 6 mm. thick. The male is 
somewhat more than half as large (Fig. 3(3). Both sexes are pointed 
at the ends, the posterior end of the male being curved into a spined 
hook. The eggs, from 0. 05 to 0. 06 mm. in diameter, are surrounded by 
an albuminous envelope (Fig. 38) and are quite resistant to destructive 
agencies. The mode of development and life history of these parasites 
are not very well understood. Their usual seat in man is the small 
intestine, but they may wander into the stomach, and exceptionally 
get into the mouth, nose, bronchi, gall passages, peritoneal cavity, 
etc. They may be single in the gut or present in great numbers. 

Two other species of ascaris have been found in man. A. Diari- 
tinia was found in the vomit of a child in Greenland, in auiiumatuiv 
condition. ^-1. nii/sfa.v, a tolerably ci^miuc^n form in c*ats ami do^-s. 



112 



PARASITES. 



has been found a few times in man. It is smaller than A. lumbri- 
coides. 

Oxyuris vemnicularis (Threadworm or Pin worm). — This spe- 
cies is very small ; the female has a pointed tail and is about 1 
cm. long. The posterior end of the male, which is about 4: mm. 



Fig. 37.— Oxyuris vermicularis. 
A, Female. B, Male. 

long, is blunt, and after death somewhat curled (Fig. 37). The eggs 
(Fig. 38) are produced in great numbers, are oval, and about 0.053 
mm. long. This parasite is very common in children, and may be 
present in large numbers in the colon. They may, in the female, 
enter the vagina and uterus. This worm is only known to infest the 
human subject, and infection doubtless occurs by the ingestion of the 
eggs, which are ^videly distributed in a variety of ways on many 
objects, fruits, etc. 

Strongylus gigas. — This is a slender red worm, the female being 
sometimes 1 metre long and over 1 cm. in diameter. It has been 






A ^3 

Fig. 38.— Eggs of Nematode Worms. 
A, eggs of Asearis lumbricoides, x about 300. B, eggs of Oxyuris vermicularis, x about 250. 

found several times in the pelvis of the kidney in man. It is more 
common in the wolf, fox, horse, seal, and some other animals. 
Strongylus longevaginatiis. — The female is about 2.5 cm. long, the 
male, as usual, shorter. It is of a yellowish- white color, and has 
been found once in the lung of a boy in Germany. 



PARASITES. 113 

Dochmius cluodenalis. — The female is from 1 to 2 cm. long, the 
male about 1 cm. long. The body of the male is dilated anteriorly 
and curved backward. Its mouth is furnished with a chitinous cap- 
sule and chitinous claws and teeth. It is found in the small intes- 
tine of man in Italy, Switzerland, Egypt, and Brazil. The head is 
burrowed into the mucous membrane^of the host, and the animal is 
nourished by the blood which it sucks out, and which is usually seen 
in its intestine. An ecchymosis is produced at the point of attach- 
ment, or even severe haemorrhage, and marked anaemia may be the 
result of the presence of large numbers of the parasites. 

Trichocephalus dispar (Whipworm). — The males and females 
are of nearly equal size, 4 to 5 cm. long. A little less than one-half 
of the body (the posterior portion) is about 1 mm. thick, and in the 
male is rolled into a flattened spiral, but in the female is but slightly 
bent. The anterior part of the body is very slender (Fig. 39) and is 
embedded in the mucous membrane of the host. The eggs are elon- 
gated, oval-shaped, about 0. 05 mm. long and about one-half as wide. 




Fig. 39.— Trichocephalus dispar. 
From the skin of the mous veneris. 

with a thick brown capsule. This parasite is very common in some 
countries, especially in France and southern Italy. It is commonly 
found in the caecum, usually in small, but sometimes in very large, 
numbers. A specimen was found by Brockway in a case reported 
to the New York Pathological Society, January, 1892, with the head 
embedded in the subcutaneous tissue of the mons veneris in a dis- 
secting-room subject of unknown history. It is usually of little 
pathological significance, commonly producing no symptoms. Its 
developmental history is not well known. 

Trichina spiralis. — The female of this most dangerous and com- 
mon parasite is, in the mature condition, about o mm. long, the male 
from 1 to 1.5 mm. long; they are filiform in shape and white in 
color. The young are born in the form of tiny worms about 0.01 
nnn. in lengtli and somewhat similar to the adult in shape. Infec- 
tion occurs in man from the ingestion of insufficiently cooked pcn-k. 
The muscle of the diseased pig contains the embryos of the parasite 
in an encysted condition. In the stomach the capsule of the worm is 



lU 



PARASITES. 



dissolved and the embryos are set free. They very rapidly mature, 
increasing in size, and the females give birth in the small intestine 
to verv laro^e numbers of vouns^. It is estimated that a sinoie fe- 
male may give birth to from 1,300 to 1,500 young. These find their 
way, through the mucous membrane and wall of the gut, into various 
parts of the body. ^ 

The exact course which thev take in o'ettino- out of the o'ut is not 
•fully established ; probably they traverse the tissues in different 
ways. At any rate, they find their way to the voluntary striated 
muscle tissue, which they penetrate, and enter the muscle fibres. 
Here they cause a disintegration of the contractile substance, and 
coil themselves inside of the sarcolemma. In this situation they be- 
come encapsulated by material in part furnished by themselves, in 
part by means of the inflammatory reaction which their presence in- 






i^-^^TSS 











.■\-,. 









SfiSs^i^^'^ 













~--^-i^gii0;-^^ii^^^vy^^|vJgJ^>^ ' 



Fig. 40.— Trichina encysted in" Muscle. 
In one capsule the parasite is dead and its remains calcified. 



duces in the connective tissue of the muscle. The worms are sur- 
rounded inside the capsule by granular material (Fig. 10). The 
capsule after a time becomes partially calcified, and in this condition 
may be readily seen by the naked eye as a tiny white speck. In this 
encysted state they may remain inactive but H^'ing for an indefinite, 
often for a very long time. Most frequently the cysts contain but 
one embrvo, but thev mav contain from two to four. The embrvo 
may dig and its remains become calcified. 

The same course of events transpires when the muscle trichinae 
are eaten by the pig or a variety of other animals. 

The embrj^os in the muscle are killed by a tem23erature of 55^ C. 
and by some of the methods of curing pork. 

The embrvos mav mature and a new sreneration be born -v^-ithin 
from five to eight days after the ingestion of the diseased meat. 



PARASITES. 115 

As the result of the presence of these parasites in the body, if 
the invasion be severe, acute catarrhal enteritis, with diarrhoea and 
vomiting, high fever, and severe pains, is apt to occur. Qildema of 
the face and of other parts of the body, broncho-pneumonia, and fatty 
degeneration of the liver may be found at the post-mortem examina- 
tion of cases which have succumbed to the disease. The encapsu- 
lated embryos may be found in enormous numbers in various volun- 
tary muscles of the body, but they are most apt to be found, when 
not very abundant, in the muscles of the neck and larynx, in the 
intercostals and the diaphragm. They tend to collect toward the 
tendinous extremities of the muscles. Trichinae also occur in the 
rat, cat, mouse, and other animals. ^ 

Filaria medinenis (Guinea worm). — This is a thread-like worm ; 
the female, which is alone known, being sometimes as much as 80 
cm. long and from 0.5 to 1.7 mm. thick. It is common in the East, 
and inhabits the subcutaneous connective tissue, in which it often 
gives rise to abscesses and ulcers. The embryos live for a time free in 
fresh water, and are then taken up by a species of fresh- water crusta- 
cean, in whose body they undergo further development, and b}' the 
ingestion of which the infection of the human subject occurs. 

Filaria sanguinis hominis. — The embryo of this parasite, which 
inhabits the blood and lymph of man, especially in Brazil, Egypt, 
and some parts of the Orient, and occasionally occurs in this coun- 
try, is about 0.35 mm. long, rounded anteriorly, and pointed at the 
tail (Fig. 41). It has about the diameter of a red blood cell. It 
occurs, sometimes in great numbers, in the blood during the night 
time, being as a rule absent during the day. It may occur in the 

^ For the examination of muscles for the detection of the presence of the parasite. 
small pieces are snipped out with tlie scissors, and squeezed into a thin sheet between 
two slides, and examined with a low power, A considerable number of bits of 
muscle should be examined, particularly from the above-mentioned favorite situa- 
tions, before excluding them in a suspected case, because they are sometimes pre- 
sent in small numbers. A thorough search is of especial importance in the examina- 
tion of pork, since, owing to the enormous fertility of the parasites, even a moderate 
number may give rise to a severe infection. 

For the minute examination of the parasite, bits of muscle should be hardened in 
Miiller's fluid and alcohol, and decalcitied if necessary, and, after embedding in cel- 
loidin, thin sections cut and stained double with luematoxylin and eosiu, and mounted 
in balsam. Bits of muscle may be also teased, the embryos picked out with a needle, 
and the cysts either broken open under a lens with the needle, or squeezed under the 
cover glass. The embryo worm thus set free may be mounted in a mixture of equal 
parts of glycerin and picric acid. The adult forms, which may be obtained by feed- 
ing rabbits with uncooked trichinous muscle, and examining after the proper in- 
terval, may be hardened in jMiillcr's fluid, and mounted in a mixture of equal parts 
of picric acid and glycerin, or in the same mixture which has been lightly tinged 
with eosin, 



116 PARASITES. 

urine in connection with cliyluria and haematiina. The mature fe- 
male is from S to 1'"' cm. lon^\ and has been found inhabitins: the 
lymph vessels of man. particularly in the scrotum and lower ex- 
tremities. Owing to the obstructions which it causes in the lymph 
ch'culation. and to the local irritation which its presence induces, it 
sometimes gives rise to lymphangiectasis. oedema, abscesses, and 
perhaps elephantiasis. One of the embryonic stages of develop- 
.nient is beheved to transph-e in the body of a species of nocturnal 
mosquito. Through the bodies of the dead mosquitoes, which are 
hable to fall into the drinking water, it is beheved that the spread of 
the parasite may occur. 

There are several other species of lilaria occasionally found in 
man which it is not necessary to enmnerate here. 

Bhahdonema strongyloides. — A small, fib form worm from 1 to 
2 mm. in length is found, often in enormous numbers, in the intes- 
tines, bihary and pancreatic ducts of man in Cochin Cliina and in 




Fig. 41.— Ftt.arta S.4KGri>as HoitEsis. 

From a case in the Xew York Hospital. The specimen was prepared and loaned to the writer 
by Dr. F. Ferguson. 

Italy, giving rise to endemic chronic diarrhoea. It has been thought 
that there are at least two species, which have been described imder 
the generic name AgiuJJjda. but recent researches by Leuckart 
have led hhn to beheve them to be different developmental stages of 

the same form, for which he suggests the above name. 

AETHEOPODS. 

The scope of this work does not permit us to enter in detail into 
the subject of external parasites, which will be found described in 
treatises on diseases of the skhi or in the general works on parasites 
referred to below. But. owing to their frequent occurrence and 
practical importance, we may briefly describe two of the more com- 
mon forms of arthropods, the "itch insect *' and the " louse.*' 

The common "itch insect" — Sarcoptes hominis [Acarus sca- 
hiei) — is shaped somewhat like a turtle, with a chitinous covering, 
and presents the general appearance seen in Fig. ■1'2. The female is 
about 0.45 mm. long, the male a Httle smaller. 

The parasite bores little timnels in the skin, in which the eggs are 



PARASITES. 



117 



laid and the young hatched. After a few days these bore fresh 
channels in the skin. For their detection a bit of the superficiaj 
layer of the skin is snipped out with curved scissors, dehydrated and 
cleared up with oil of cloves, and examined under a low power, when 
the tunnels and the parasites, if present, will be readily visible. 

The head louse, Pediculus capitis, is from 1 to 2 mm. long, the 
female being slightly the larger. The general appearance of the in- 
sect is seen in Fig. 43. 

MODES OF STUDY AND PREPARATION OF THE ANIMAL PARASITES. 

The methods of studying the protozoa have been given above, 
page 105. 

The smaller and embryonic forms of the various kinds of para- 
sitic worms may be hardened, best under the cover glass, with 









Fig. 42. 



Fig. 43. 



Fig. 42.— Sarcoptes Hominis— the *' itch insect " Female: back view. After Fiirstenberg. 
Fig 43.— Pediculus Capitis— the "head louse." Male. After Braun. 

Miiller's fluid or osmic acid, and these may be, when the hardening 
is completed, replaced by dilute, and this by strong alcohol, and the 
latter finally replaced by eosin-glycerin, in Avhich the specimens are 
permanently preserved ; or they may be stained lightly by tinging the 
alcohol with eosin, and then cleared up by oil of cloves, and finally 
mounted in balsam. 

It is necessary, however, for detailed study of the larger para- 
sites, to make thin longitudinal and transverse sections from dif- 
ferent parts of the body. This c;ui be readily done, even in vor\' 
small forms, by embedding the aninird — after careful hardening in 
osmic acid or in Miiller's fluid, and afterward in alcohol — in cel- 
loidin, and using the microtome. The sections may be stained 
double with luiematoxylin and eosin, and mounted in balsam. 

The general arrangement of the generative organs in the i>roglot- 
9 



118 PARASITES. 

tides of tapeworms may be well seen by staining in eosin or eosin- 
glycerin after moderate hardening in dilute alcohol, and then 
squeezing the segment between two glass slides. The itch insect 
and louse may be soaked for a few hours in turpentine and mounted 
in balsam/ 

^ Bibliography. — Especially to be recommended for detailed description of human 
animal parasites, together with practical suggestions for their study, is tlie small 
work of Braun, "Die thierischen Parasiten des Menschen," 1883, which contains 
also the more important older bibliography. 

The more extended classical works of Cohhold, " Entozoa of Men and Animals," 
1879, and KiXchenmeister and Zilrn, " Die Parasiten des Menschen," 2d ed., and the 
work of Leuckart, "Die menschlichen Parasiten," should be consulted, and contain 
valuable bibliography. Various forms of external parasites of men and animals are 
fully described and illustrated in the work of Megnin, ' ' Les parasites et les maladies 
parasitaires chez I'homme," etc., 1880. The plates of Stein, illustrating the Cestoda, 
1882, are carefully executed. In the " Report on Trichinae and Trichinosis,"' in 1880, 
by Glazier, Surgeon in the Marine Hospital Service, will be found an illustrated ac- 
count of the natural history of this parasite, history of the disease, etc., and a section 
on its occurrence in the United States. 



VEGETABLE PARASITES. 



The vegetable parasites of man belong among the lowly forms of 
plants, three distmct forms of which are of frequent occurrence in or 
upon the body. These are : 

1. Bacteria, or fission fungi (Schistomycetes). 

2. Yeasts, or yeast fungi, or sprouting fungi (Saccharomycetes). 

3. Moulds, or mould fungi (Hyphomycetes). 

The first group, the bacteria, is of the greatest significance, be- 
cause it contains organisms which are very frequently the cause of 

serious disease/ 

I. BACTERIA. 

Morphology and Physiology. — Bacteria are minute vegetable 
organisms of the lowest and simplest form, allied to the algse. They 
are widely distributed in the air, water, and surface soil, and are par- 
ticularly abundant among the habitations of men, or wherever ani- 
jiial and vegetable substances are undergoing decay. 

Bacteria of one kind or another are invariably present in greater 
or less numbers in the mouth, nose, upper air passages, and gastro- 
intestinal canal of men and animals. The largest of them are too 
small to be seen with the naked eye, and the smallest require for their 
recognition the most perfect and powerful of our microscopic aids. 
They have various shapes : spheroidal, rod-like, filiform, or spiral 
(Fig. 44). They are simple cells, formed of a membrane enclosing 
the protoplasm, which may appear homogeneous or granular. A 
nucleus has been demonstrated in several forms, but this it is difficult 
to see owing to the extreme minuteness of the cells. They are some- 
times single, sometimes grouped together in varying ways and num- 
bers. • * 

When the conditions are favorable the bacteria multiply by 
transverse division, often with extraordinary rapidity, so that from a 
single germ large numbers may be produced, each of which in turn 
may by division or fission contribute to the increase in numbers. Each 



^ The term micro-oi^ganism includes all of these forms of minute and lowly plants. 
They are also sometimes spoken of collectively as germs. 



120 VEGETABLE PARASITES. 

indi\'idual after the dh^sion grows out into the original form and 
size. Not infrequently after the production of new individuals by 
fission these do not fall apart, but remain grouped or attached to one 
another in a more or less characteristic way ; some in pairs or chains, 
some in irregular masses, some in masses embedded in gelatinous 
substance and then called zoogloea colonies. We thus have what 
are sometimes called '^ growth groups ''of bacteria. This growth- 




Fig. 44.— Drawing op three typical Forms or Bacteria illostrating the three Classes. 
Stained with fuchsin. 

grouping is often so constant and characteristic that it has been used 
as a basis for nomenclature (see below, page 139). Some bacteria 
are surrounded by a broad, homogeneous envelope called a capsule 
(Fig. 45). 

Under a variety of conditions, the limitations of which .are not 
very v^ell understood, new bacteria are produced, and the species is 






(%\.^« -* 

^4" 






Fig. 45.— Bacteria with Capsule. 



perpetuated, not by simple division, but by the development of spores. 
The most common mode of spore formation is called endogenous. 
A small, shining mass makes its appearance within the protoplasm 
from which it is formed, grows more and more distinct, and finally 
appears as a sharply defined spheroidal or oval, strongly refractile 
body (Fig. 46), which can be separately stained and may remain 
^vithin the old cell membrane or free itself. Only one spore develops 
in a single germ. Their formation has been observed in rod-like and 
spiral bacteria only. The spores appear to be surrounded by a dense 



VEGETABLE PARASITES. 121 

envelope, and are, as a rule, much more resistant to deleterious agen- 
cies than are the bacteria themselves. Vacuoles in bacteria are often 
mistaken for spores. Spores, when placed under favorable conditions 
in the presence of moisture and nutriment, swell, become less retrac- 
tile, and develop into the usual vegetative form. Another mode of 
sporulation — arthrogenous — has been described, but its nature is not 
well understood, and even its occurrence is doubted by many. 

Some bacteria are and some are not very sensitive to changes of tem- 
perature. At a temperature below + 5° C. they are incapable of activity 
or proliferation, but some forms are not killed by a temperature of — 1 11 ^ 
O. As the temperature is raised their activities increase up to a cer- 
tain point. It may be said in general that they are most active at 
about the temperature of the body, although species differ consider- 
ably in this respect. In fluids many bacteria are killed by a pro- 
longed exposure to a temperature of from 60° to 70° C, and all are 
killed by a temperature of 100° C. (the boiling point of water) if this 
be long enough continued. When dry they resist much higher tem- 




FiG. 46.— Bacilli showing Spores. 
The bodies of the bacilli are stained with methylen blue, the spores with f uchsin. 

peratures than when moist. The spores are, as a rule, more resistant 
to high temperatures than the bacteria themselves, some having been 
exposed, dry, to a temperature of 140° C. without destruction of life. 
Fluids containing the spores of bacteria which resist very high tem- 
peratures may be sterilized by boiling for a short time, then being 
allowed to stand at ordinary temperatures for several hours, and then 
again boiling; this process being repeated several times In this way. 
although the spores themselves are not killed by the heat, the bac- 
teria into which they develop during the intervals are killed, so that 
finally the medium is entirely freed from both living spores and adult 
bacteria. 

Strong light is in general inimical to the life and growth of 
bacteria. 

Certain disinfecting agents, when brought into contact Avith bac- 
teria, are capable of greatly reducing their activities or destroWug 
them altogether ; but different forms differ greatly in their power of 
resisting the action of these agents. The spores of certain bactoria 
are exceedingly resistant, much more so than the bacteria themselve^i. 



122 VEGETABLE PARASITES. 

to the action of disinfecting agents. Among these disinfectants may 
be mentioned carbohc acid, and especially solutions of corrosive sub- 
limate, which is very inimical to the life of most bacteria and their 
spores, even in extremely dilute solutions. 

Some bacteria are capable of performing rapid movements, others 
are not; and the same form may be at one time mobile and at another 
immobile, depending upon external conditions. Movement is largely 
confined to the rod-like and spiral forms, but has been observed in 
the spheroidal. Many bacteria have one or more cilia, by means of 
whose vibrations they perform their active progressive movements 
(Fig. 47). 

It has been shown that certain of the motile bacteria, when sus- 
pended in fluids, are attracted toward, or repelled from, chemical 
substances dissolved in water. This is called chemotaxis. 

Putrefaction and putrefactive products are always dependent upon 
the presence and activity of bacteria. They require for their nourish- 




FiG. 47. —Bacilli, showing Cilia. 

ment nitrogen and the h5^drocarbons ; oxygen is necessary for the 
proliferation and activities of some forms, and for others not. 

Those bacteria which require free oxygen are called aerobic. 
Those which do not grow in its presence are called anaerobic. But 
between these extremes there are forms which make shift to grow 
without oxygen under favorable conditions, though they make use 
of it when present ; others which may grow in its presence, though 
flourishing best in its absence : these are called facultative aerobes 
or facultative anaerobes, in distinction from, those first mentioned, 
which we call obligatory aerobes or anaerobes. 

Bacteria are active only in the presence of moisture ; but when 
this and other conditions favoring their activity fail they do not 
necessarily die, but some forms may remain, either as spores or as 
fully developed organisms, for long periods wholly dry and inert, 
but capable of resuming their activity whenever they are again re- 
stored to favorable conditions. 

The bacteria play a very important role in nature in virtue of 
their power of feeding upon and pulling to pieces dead organic 



VEGETABLE PARASITES. 123 

materials. A small part of the new chem.ical compounds which are 
thus formed are used by the bacteria themselves for the purposes of 
their own nutrition and growth, while the rest are set free to serve, 
sooner or later, as food for other forms of plants or animals. Bac- 
teria grow best, as a rule, when in an organic food medium which is 
neutral or slightly alkaline. 

A large number of complex chemical substances are elaborated 
during the growth of bacteria, their nature varying with the species 
of bacteria and the composition of their nutrient material. 

Some of the chemical compounds set free by the growing bacte- 
ria are bad-smelling or aromatic gases ; some are inert and harmless 
substances ; some are powerful poisons, and may, when they have 
accumulated in the fluids where they grow, destroy the bacteria 
which have produced them. Many bacteria produce brilliant coloring- 
material as they grow. Certain of the basic chemical compounds 
resembling the vegetable alkaloids, which are formed by the action 
of bacteria in organic matter, are called ptomains. ' The ptomains 
of certain special forms of bacteria ar« believed to be of great import- 
ance in inducing the deleterious effects of many infectious diseases ; 
these are called toxins. Complex proteid bodies may be produced 
during the growth of bacteria ; these may be in part set free, in part 
become assimilated in the bacterial cell protoplasm. These proteid 
bodies belong in part to the albumins, in part to the albumoses, 
while some of them resemble the peptons. Many of them seem to 
be most potent factors in the induction of the phenomena and le- 
sions of the infectious diseases. The poisonous albuminous sub- 
stances produced in the body by the growth of certain disease-pro- 
ducing bacteria are called toxalhurnins. 

THE RELATIONS OF BACTERIA TO DISEASE. 

Bacteria of various forms may occur on the surface of the skin 
and mucous membranes, and in the lungs, exerting no apparent in- 
fluence whatever, so far as we can judge by morphological appear- 
ances, upon the surrounding parts. They may occur on the surface 
of wounds, ulcers, etc., without the production of any evident 
changes ; they sometimes lie within cells which appear otherwise 
perfectly normal. Bacteria of various kinds may be put into the 
body, and even into the blood, without doing harm. This is probably 
because either the food or conditions of growth are so ill-suited to 
their special requirements that they cannot grow and proliferate, or 
because some substance which they encounter in the tissues or the 



' LeiiGomaines are basic products produced iu the tissues of liviug luiimuls by nio- 
tabolism. 



124 



VEGETABLE PARASITES. 



body juices is inhibitory to their gTOTvi:h; or kills them outright — is, in 
other Tvords, bactericidal. 

On the other hand, the cells and tissues in the ^dcinity of bacte- 
ria which have gained access to the body may show very marked 
alterations, which are presumably due to their influence. The cells 
may be swollen, their nuclei may break do^vn or disappear, and the 
protoplasm may be converted into . a mass of shining or coarsely 
granular particles, or may completely disintegrate. The intercellu- 
lar substance near the bacteria may also soften and disintegrate. In 
a word, the tissue in their immediate vicinity is often found in a 
condition of necrosis of one kind or another. The walls of blood 




Fig. 48.— Bacterial EireoLrs in the Blood VesseIxS of the GLOMERiTLrs of the Kldijey in 
Malignaxt Ulcerative Endocarditis. 



vessels near which they lie may die, and the blood which these carry 
may form thrombi. The bacteria may themselves enter the vessels 
and prohferate in the blood : they may be swept away as emboH to 
remote parts of the body (Fig. 48), and establish new foci of bacte- 
rial prohferation and tissue necrosis. Some forms, instead of caus- 
ing the immediate death of the tissue, appear to incite inflammatory 
changes about themselves (Fig. 49). These may be simple and 
similar to those produced by the presence of any irritating foreign 
body : or it would seem that the bacteria may determine, in some 
way as yet imknown to us, very peculiar and characteristic inflam- 
matory changes which may result in the formation of new tissues 
of various kinds (see Tuberculosis). Some forms of bacteria find in 



VEGETABLE PARASITES. 



12o 



the blood, others in the lymph spaces and vessels, the conditions 
most favorable for their proliferation. 

When we inquire more closely into the exact way in which these 
various deleterious effects are produced in the body by pathogenic 
bacteria, we find that they are in but small measure simply mechan- 
ical. They appear to be largely due to the various chemical pro- 
ducts eliminated or stored up in their protoplasm by the metabolism 
of the germs. These deleterious bacterial products may be those 
alkaloidal substances called poisonous ptomains or toxins, or they 




Fig. 49.— Colonies of Micrococci in a Blood Vessel op the Kidney, causing a small 
Abscess. From a case of pyaemia. 

Around the dilated aud partially necrotic blood vessel in which the bacteria lie is an area of 
necrotic tissue and a small-celled infiltration or zone of pus. 



may be albuminoid substances — toxalhumins or toxaJhiinioscs. 
Stored up in the protoplasm of the germs themselves, this poisonous 
material has been called bacterial protein. 

The chemical constitution of these varied products is so complex 
and little understood, and the conditions under which they are devel- 
oped, and the parts of the body to which they are spread and on 
which they may act, are so varied, that it is not possible to make very 
positive statements to-day as to their individual characters or the 

10 



126 VEGETABLE PARASITES. 

nature of their action.' Some of the poisons act locally at or near the 
seat of their manufacture by the growing germs. Others gain access 
to the body at large and are widely distributed, inducing what may 
be called the phenomena of septic intoxication. 

The phenomena of septic intoxication may be induced by the pro- 
ducts of bacterial growth outside of the body when these in con- 
siderable quantity are in any way taken in. This is true not only of 
■poisons elaborated outside the body by pathogenic bacteria, but also 
of many forms of bacteria usually harmless. Thus are caused many 
forms of food poisoning which simulate but are not actually infec- 
tious diseases, because there is no development within the body of 
the disease-producing germs. 

It has been found that the proteid constituents of the protoplasm 
of various species of bacteria, both parasites and saprophytes, are ca- 
pable, when set free by the disintegration of the germs in the body, 
of attracting leucocytes in large numbers to their ^dcinity. This 
drawing of living cells by chemical agents is called chemotaxis,^ and 
it seems probable that the gathering of cells in suppurative foci ma}^ 
be due to the chemotactic power of the bacterial protein of the disinte- 
grating germs which have gathered there. ^ This chemotactic powder 
is not confined, however, to the bacterial protein, but is exhibited by 
proteids from a great variety of sources. It has furthermore been 
sho^vn that bacterial proteids are capable of stimulating cell prolif- 
eration. This has been shoAvn in the case of leucocytes and many 
other forms of cells (see action of the bacterial protein of • the tu- 
bercle bacillus, page 176). 

It will be seen, from what has now been said of the bacteria, that 
in different parts of the system in health, and in a large number of 
diseased conditions, various forms of bacteria occur ; but it is quite 
evident that the significance which we must attach to their mere 
presence varies greatly. In a large number of cases, especially when 
on parts exposed to the air or in the gastro-intestinal canal, they are 
evidently of no more importance than so much inorganic dust. 
When, however, special forms of bacteria are found to occur uni- 
formly in connection with well-defined diseases, or in their lesions, 
the conjecture is certainly justified that they may have something to 
do with their production. Yet in all such cases we have to consider 

^ Much of the literature on this subject has been brought together by Vaughan 
andNovy, "Ptomaines and Leucomaines." 2d edition, 1891. Tlie general chemical 
relationship of bacterial products to other organic compounds is set forth in Hallibur- 
ton s " Text Book of Chemical Physiology and Pathology." , 

^ Negative chemotaxis is the repelling of living cells by chemical substances. 

■^For a resume of observations on chemotaxis see New York Medical Journal, 
June 6th, 1891. • 



VEGETABLE PARASITES. 127 



\! 



the possibility that it is the diseased state or the character of the 
lesion, produced perhaps by other causes, which affords conditions 
suitable for bacterial growth, and that they may consequently occur 
in considerable numbers, while in the absence of these conditions 
they would be unable to develop. Even the constant occurrence in 
the body, in certain diseases, of bacteria Avhich evidently produce 
well-marked local effects, either inflammatory or degenerative, does 
not absolutely prove their causative relation to the disease, although 
it renders it to a certain degree probable. 

In order to absolutely prove the bacterial origin of an infectious 
disease, we must not only be able to demonstrate the constant pre- 
sence in the body at some time of a special form of bacteria, but we 
must obtain them in an absolutely pure condition, unmixed ^vith any 
other living thing, or with any chemical substance not belonging to 
them, and, by the introduction of the purified organisms into a 
healthy animal, be able to produce the disease in some definite form. 
When all this is done, and not before, can we assert with absolute 
certainty the causative relation between a given form of bacteria and 
any special infectious disease. But the fulfilment of these strict re- 
quirements is very difficult in many cases, and in some, apparently, 
almost if not quite impossible ; for we must remember, in the first 
place, that the lower animals, upon which alone, for the most part, 
inoculation experiments are practicable, are apparently not subject to 
certain important diseases of man ; and, second, that they present 
among themselves the most marked differences in the degree and 
manner in which they are affected by the inoculation of pathogenic 
bacteria. Desirable as is the complete fulfilment of the above re- 
quirements in every case, it must be admitted that a reasonable cer- 
tainty regarding the bacterial origin of a given disease may be 
arrived at without positive results from the inoculation of the bac- 
teria associated with its lesions. 

The discussion of the probabilities of the bacterial origin of certain 
classes of disease, and the long series of phenomena exhibited by 
them, which the bacterial theory very satisfactorily explains, does 
not fall within the scope of this book. 

The complete demonstration which certainty requires has as yet 
been furnished in but a moderate number of cases. In a consider- 
able number of other cases, although the complete cycle of proof has 
not 5^et been established, enough has been done in the way of study 
and experimentation to render it altogether probable tliat certain 
forms of bacteria are the cause of the diseases. 

Conditions Injiuowiug tJie Occurrence of Bacterial Pis- 
eases. — It has been learned, as the result of a, great deal of observa- 
tion and experiment, tha,t although certain diseases are invariablv 



128 VEGETABLE PARASITES. 

caused by the presence and growth in the body of particular species 
of bacteria, and never occur without them, still there are various 
other accessory factors which have a very important bearing upon 
the inception and course of the diseases. Thus, while the presence 
in the body of a particular species of bacteria is the most significant 
and fundamental of the determining agencies in the bacterial dis- 
eases, the numbers in which they are present — i. e. , the size of the 
.dose — and the varying virulence which the same species under dif- 
ferent conditions possesses, as well as the varying capacity of re- 
sistance to the incursions of the germs which the body cells at 
different times and under differing conditions exhibit, are all factors 
of the greatest moment. 

It should be always borne in mind that the human body is a 
grea.t aggregate of groups of co-ordinated cells which, under nor- 
mal conditions, all act in harmony for the maintenance of the life 
and functions of the individual. The cells and cell communities 
in health not only do this, but they have the power of resisting and 
to a certain extent overcoming the various deleterious agencies to 
which the body is more or less constantly liable. 

What we call hereditary or acquired predisposition to a bacterial 
disease, such as tuberculosis, for example, is simply a lack of the 
usual capacity of the cells of the body— whether through a struc- 
tural or physiological fault we do not yet know — to cope with the de- 
structive tendencies of the living bacteria when once these gain a 
foothold in the body. 

We thus see that, in studying the conditions under which bac- 
terial diseases occur, the work is by no means complete when we 
have demonstrated the bacterial species which causes the disease, but 
that then the more obscure determining and influencing agencies 
must be worked out in each particular case. 

IMMUNITY AND HEALING. 

The fact that all animals are not equally susceptible to the 
ravages of pathogenic bacteria, and that in man an individual and 
often changing predisposition or invulnerability to the incursions of 
these organisms exists ; the further observation that one attack of an 
infectious disease often protects the victim for a longer or shorter 
time against a recurrence ; finally, the very fact that recovery is 
possible when once self -multiplying disease-producing germs have 
obtained a foothold in the body — all these facts and observations are 
of such singular import and interest that, especially of late years, 
much theorizing and much study have been expended on the nature 
of the forces which the body cells bring into play in establishing im- 
munity and predisposition in the face of bacterial invasion, and in 



VEGETABLE PARASITES. 129 

coping with the various poisons formed when once a foothold is ob- 
tained. The scope of this book does not permit us to enter in detail 
into this most fascinating and important field. 

It is believed by many that certain cells of the body are capable 
of taking up bacteria, which get into the tissues, into their proto- 
plasm, and there killing and perhaps digesting them, and that thus 
the destruction of bacteria in the body may be brought about. The 
cells which take up into their bodies the bacteria, as well as other 
foreign bodies, are called phagocytes. This assumed mode of de- 
struction of bacteria forms a most suggestive and fascinating 
hypothesis, but its significance and importance are not yet fully de- 
monstrated. 

On the other hand, certain albuminous ingredients of the body 
juices have been shown to possess marked bactericidal poAvers, which 
may be of extreme importance in protecting the organism against 
the germs. But how important this is we cannot yet say. 

While thus two fairly distinct influences are alleged to be of 
importance in enabling the body to resist the incursions of patho- 
genic germs — the cellular or *' phagocytic" and what may be called 
the ^'humoral" — it is obvious that ultimately whatever protecting 
power the body possesses must be due, directly or indirectly, to cell 
activities. 

Very recently a new point of view has been reached as the result 
of much experiment, which seems to indicate that in the presence 
of the poisonous substances which bacteria elaborate when groA\4ng 
in the body, the cells or body juices themselves may develop the 
power of forming an antagonizing material. In this case the pro- 
tecting agency is not bactericidal, but renders inert the poisons by 
which alone or largely the bacteria cause harm. The body, under 
these conditions, does not become, strictly speaking, immune, because 
the bacteria may go on growing, but it does become, so to speak, 
''poison-proof." Recent experiments on pneumonia, tetanus, and 
other infectious diseases would seem to indicate that the body may 
be rendered by artificial means " poison-proof," and thus a new and 
promising line of treatment of the infectious diseases is suggested. 
The conf errence of artificial immunit}" by means of the introduction 
into the body of bacterial products of one kind or another has been 
well established by many observers. But the subject is far too com- 
plex and too little understood to justify us in pursuing it further here. 

The reasons for believing that certain well-known and important 
diseases are caused by bacteria, as well as a description of the par- 
ticular organisms concerned, Avill be found in that part of this book 
which treats of the Infectious Diseases. 



130 VEGETABLE PARASITES. 

:^IETHODS OF STUDYIXG BACTERIA. 

The simplest mode of studying bacteria is to exam^ine them either 
in the fluids in Trhich they he or in one-half -per-cent salt solution. 
and for the study of many of the phenomena of hf e this method is 
important. The tissue and other elements, ho^vever, ^th which 
thev are often associated ^reatlv interfere with the studv of the bac- 
teria. and manv forms are so small as to be scarcelv recooniizable in 
the natural condition. 

By far the most important aid in the morphological study of the 
bacteria is derived from the use of staining agents. Most of the bac- 
teria are stained more or less readily by one or more of the anilin 
dves. The ease vrith which thev are colored varies considerably in 
different species and with the different dyes. The tissue elements. 
and a variety of other materials "with "which the bacteria may be as- 
sociated, also stain more or less readily at the same time : but most 
of these part with their color more readily than do the bacteria on 
being treated with alcohol or dilute acids. We are thus enabled to 
obtain a differentiation in color between bacteria and other structures. 
The bacteria, moreover, differ among themselves in respect to the te- 
nacity with which they hold then' stain in the presence of decoloriz- 
ing agents, and upon this fact is based one of the important methods 
of distinguishing between different species. 

A m ong the anilin dyes more co mm only empLjyed for bacteria 
stainino: mavbe mentioned f uchsin. o:entian violet, andmethvlen blue 
\ saturated alcoholic solution of these dyes should be kept in a 
tightly stoppered bottle, and from this the more dilute solutions re- 
quired for staining may be prepared. For ordinary purposes one 
part of the alcohohc solution of fuchsin or gentian violet, added to 
twenty parts of water, will give a staining solution of suitable 
strength. This should be prepared in small quantities as required, 
since it does not keep well and a granular precipitate is apt to form 
in a few days. 

Special stains and modes of staining, such as are necessary for 
some forms of bacteria — the tubercle bacillus, for example — ^vill be 
described under the appropriate headings. AVe are speaking here 
only of the general methods. 

To Stain Bacteria in Fluids. — A small drop of the fluid is placed 
on a cover glass, spread a httle with a needle, and allowed to dry by 
evaporation in the air or by gentle heating high over a flame. The 
cover glass is now held with the forceps, and, specimen side up, 
passed moderately rapidly three times through the flame of an alco- 
hol lamp or a Bim.sen burner. The material on the cover should not 
be burned. This heating not only flxes the contents of the fluid 



VEGETABLE PARASITES. 131 

lirmly on to the glass so that it will not easily soak off, but it ren- 
ders insoluble any albuminous materials which may be mixed with 
the bacteria, and which might otherwise interfere with subsequent 
examinations by forming granular precipitates. 

A drop of the aqueous staining fluid is now put on to the dried 
specimen on the cover glass, and if this be held in the forceps and 
tilted slightly up and down a few times so as to bring fresh portions 
of the staining fluid into contact with the bacteria, the staining will 
usually be completed in two or three minutes. The stain is now 
washed off with a jet of water from the wash bottle, and the speci- 
men is either mounted directly in a drop of water for temporary 
study, or the washing water is drained off and, after drying in the 
air, is mounted directly in balsam. 

It is well to use balsam which has been softened, when this is 
necessary, with oil of cedar or xylol, since chloroform is apt to de- 
colorize the bacteria. 

If the bacteria which are to be stained are in solid masses, as is 
apt to be the case in pure cultures on solid media (see below), a 
small drop of distilled water should be first put on the middle of the 
cover glass, and a very minute quantity of the bacterial mass rubbed 
into it with a platinum needle and then dried and stained as before. 

To Stain Bacteria in Tissues. — The tissues should be well hard- 
ened in alcohol. Thin sections are placed in the above-described 
coloring solutions, where they may remain from five to fifteen min- 
utes. In some cases a much longer staining is necessary. Gentle 
warming (40° to 50° C) will hasten the staining. The entire tissue 
as well as the bacteria is in this way deeply colored. The sections 
are rinsed with distilled water and then placed in alcohol. This, 
with varying degrees of rapidity with different stains and tissues, 
gradually extracts the color from the tissue, most slowly from the 
nuclei. The time required and the exact degree of decolorization to 
be sought for must be learned by experience in different cases. Some- 
times five, sometimes thirty minutes are required, sometimes only 
a few seconds. It is often necessar}^ and the decolorizing of the 
tissue is thereby hastened, to add a few drops of acetic acid to the 
alcohol. When acetic acid is used it should be finally thoroughly 
washed out by alcohol. The specimens are now cleared up by oil of 
cloves and mounted in balsam. Oil of cloves removes the color 
from some forms of bacteria, and in this case xylol or oil of berga- 
mot should be substituted for it. In specimens preparetl in tlie 
above way, the nuclei of cells usually retain to some extent a color 
similar to that of the bacteria, but their size and shape serve for the 
differentiation. 

A much more generally useful method of •staining bacteria in the 



132 VEGETABLE PARASITES. 

tissues than that just given, although not in all cases apphcable, is 
that known as Gram's method. The tissues from which the sections 
are made should have been hardened and preserved in alcohol. The 
sections are stained for from two to four minutes in anilin-gentian- 
violet solution. This is prepared as follows : 1 c.c. anilin oil is 
added to 20 c. c. distilled water ; this mixture is well shaken, and the 
excess of anilin oil is filtered off through a moistened paper filter. 
To the clear filtrate saturated alcoholic solution of gentian violet is 
added until the fluid becomes opalescent (about 1 part of the dye to 
10 of the water will usually be enough). A small quantity only of 
this fluid should be prepared at once, as it does not keep very well. 

From the staining solution the sections are transferred direct^ to a 
solution of iodin in potassium iodid and water (I 1.0 — KI 2.0 — H^O 
300.0). In this they remain from one to three minutes, a precipitate 
forming in the solution and the sections becoming of a dark-reddish 
or slate color. The sections are now transferred to absolute alcohol, 
which should be changed two or three times so as to dehydrate the 
specimen, which at the same time will lose much of its color. Final- 
ly the decolorization is completed and the section cleared up by oil of 
cloves, and it may then be mounted in balsam. Very little color 
should be visible to the naked eye in the specimen when it is ready 
to mount. If the specimen have been embedded in celloidin for the 
purpose of section cutting, this will be dissolved from the sections by 
the oil of cloves. Then it is well to use a second portion of oil of 
cloves, so as to get rid of the superfluous half -dissolved celloidin. It 
is also well to tint the oil of cloves lightly with a few drops of alco- 
holic solution of eosin, and then the violet-colored bacteria will stand 
out in sharp contrast with the reddish tissue elements. The iodin 
solution should never be used a s econd time, and a platinum needle 
should be used in manipulating the sections, since steel instruments 
are injured by the iodin. 

Some bacteria are decolorized by Gramas method of differentia- 
tion. 

Weigert's Modification of Grain's Method. — ^The sections are 
laid for half an hour in the anilin-gentian-violet solution prepared 
as above, then rinsed off in three-quarter-per-cent salt solution and 
spread on a slide. They are now dried with blotting paper and 
covered for two minutes with the iodin solution. The iodin solu- 
tion is now removed with blotting paper and the sections decolor- 
ized with anilin oil or a mixture of 2 parts of anilin oil and 1 part of 
xylol, several times renewed. Finally the sections are cleared in 
xylol and mounted in balsam. 

In many cases it is well to accomplish a double staining by a 
preliminary contrast stain. Thus, before the use of Weigert^s modi- 



VEGETABLE PARASITES. 133 

fication of Gram's stain the sections may be put for half an hour in a 
solution of picro-carmin, then rinsed in water and stained as above. 
A very valuable and powerful stain for bacteria, either in fluids 
or in tissues, is that known as Loffler's alkalin-rnethyl-hlue solu- 
tion, consisting of — 

Saturated alcoholic solution of Methyl Blue. . . 30 parts. 
Aqueous solution of Caustic Potash 1 : 10,000 . . 100 '' 

For staining bacteria in tissues the stain is allowed to act for a. 
few minutes. The section is then put for a few seconds in one-half- 
per-cent acetic acid, then rinsed in water, and the superfluous color 
removed from the tissue by repeated rinsing in alcohol, which at the 
same time dehydrates it. Then it is cleared with oil of cedar and 
mounted in balsam. Care should be taken not to remove too much 
color with the alcohol. For staining bacteria in fluids when there 
is little solid material other than the germs, it is used as are the 
ordinary simple anilin dyes, as described above. 

It should always be borne in mind in staining the bacteria that 
great exactness is not necessary either in the strength of the coloring 
solutions or in the time of exposure of the bacteria to them. We 
are seeking for certain effects — namely, the staining of the germs — 
and this depends not only upon the quality and strength of the dye, 
the time of exposure, etc., but also upon the nature of the bacterial 
species and its condition at the time the staining is attempted. Thus 
it not infrequently happens that bacteria which will stain readily and 
deeply with a given solution when they are in a condition of active 
growth, may scarcely be at all colored if they have been dead or in- 
active for a long time, although their outward shape appears to be 
unchanged. So it should be remembered that, while there is little 
difficulty in most cases in staining the bacteria, the operation is not 
one of mere routine, but requires intelligent attention to the particu- 
lar conditions of the species in hand. 

The Microscope. — For the recognition and study of bacteria, es- 
pecially of the minuter forms, the best optical apparatus is requisite. 
With good high-power dry lenses a certain amount of instructive 
observation on the bacteria may be made. But for finer study and 
research homogeneous immersion lenses (at least one-twelfth) must be 
used. 

A special mode of illumination is also almost indispensable for bac- 
terial work, such as may be obtained by the use of the Abbe condenser. 
The structural outlines which the tissue elements present in ma in- 
cases greatly interfere Avitli the observation of the color by which the 
stained bacteria are recognized. This interference is considerably re- 
duced by mounting the specimens in balsam, but usually not sufli- 
11 



134 VEGETABLE PARASITES. 

ciently so for the study of the minuter forms. The Abbe condenser is a 
combination of lenses, placed close beneath the object, by means of 
which, owing to the direction in which the rays of light are brought 
upon the object, structural outlines are made to nearly entirely dis- 
appear, and in this way the stained objects, the bacteria, stand out 
much more distinctly than would otherwise be the case against the 
nearly homogeneous background. 

ARTIFICIAL CULTIVATION OF BACTERIA. 

For the complete investigation of the different forms of bacteria, 
particularly in their relations to disease, we must isolate them so as 
to be able to study their life history and the effects of their inocula- 
tion into healthy animals. It has long been known that bacteria 
could be cultivated in a variety of artificially compounded, so-called 
nutrient media or soils. Fluids were formerly used for this purpose, 
but it is very difficult to separate single species in fluid media, and to 
detect contaminations when they occur. Moreover, the inevitable 
mechanical disturbances of the fluid prevent, for the most part, the 
formation of gross characteristic appearances in the masses of grow- 
ing bacteria. Dr. Robert Koch introduced, a few years ago, a tech- 
nical improvement of inestimable value in suggesting and formulat- 
ing the details of using solid media for the cultivation of bacteria. 
Among these may be mentioned sterilized boiled potatoes and gelat- 
inized infusions of various natural or artificially compounded sub- 
stances sterilized by heat. Different species of bacteria often- require 
different nutrient media, and some require different temperatures 
for their most flourishing growth. They usually grow on the sur- 
face of the nutrient media in sharply circumscribed masses, and dif- 
ferent species may grow side by side in the same receptacle for con- 
siderable periods without in the slightest degree interfering with 
one another or tending to mix. The mode of growth and general 
appearances of the proliferating bacterial masses on the solid medium 
often present very characteristic differences between different forms, 
and thus not only furnish valuable means of identifying species, but 
render possible an early detection of contamination from chance ad- 
mixture of species. A given species of bacteria may be cultivated 
through a series of generations by transferring, with proper precau- 
tions, a minute portion from a growing colony to a fresh surface of 
sterilized soil. After cultivation through several generations the 
species may be presumed, and by microscopical examinations proved, 
to be entirely pure, and the effects, if any, produced by its inocula- 
tion into healthy animals, to be due to it alone. 

The Preparation and Use of Culture Substances. — There are 
many culture media, some of which are best suited for one, some 



VEGETABLE PARASITES. 



13o 



for another species of bacteria. Those most commonly used are 
beef tea, beef tea rendered soHd by gelatin or agar-agar (called 
"nutrient gelatin" or ''nutrient agar"), boiled potatoes, coagulated 
blood serum, and milk. 

Potatoes. — The potato is scrubbed with a brush under the water 
faucet and the ends cut off with a knife, leaving a segment about 
an inch and a half long. With a tin cylinder about an inch in 
diameter, made like an apple corer, a cylinder is cut lengthwise 
out of the potato segment, and this is divided lengthwise with the 
knife into two oblique sections. These pieces of potato, after ly- 
ing for a few minutes in running water to prevent subsequent dis- 
coloration, are placed, the narrow end up, in large test tubes about 
five inches long and a little more than an inch wide, which have 
been plugged at the mouth with cotton, and freed from all germs 
which might have been upon or in them — i.e., sterilized — by heating 
in an oven for an hour at 160° C. Several of the potato tubes thus 
prepared are now put together in an open wire basket and steamed 




•^^ 



Fig. 50. — A Potato CuiiXURE 

Growing in a sterilized tube plugged with cotton. The red mass or "colony" on the oblique 
surface of the potato is made up of myriads of bacteria. 



for an hour, and again for an hour on the following day. They 
are now ready to be sown with the bacteria on the oblique surfaces 
(see Fig. 50). 

Nutinent Gelatin. — One pound of lean beef is chopped* fine, 
stirred into one litre of water, covered, and set away in the refrige- 
rator for twelve hours. The red fluid is now completely separated 
from the meat by squeezing through a cloth into an enamelled 
saucepan, which fits into a larger vessel serving as a water bath. 
To the beef juice are added ten per cent of clear French gelatin, one 
per cent of beef pepton, and one-half per cent of common salt. The 
mixture is now heated in the water bath until the gelatin is dis- 
solved, when it is carefully neutralized by the addition of a sufficient 
(quantity of a saturated aqueous solution of sodium carbonate or a 
solution of caustic soda. It should be made exactly neutral or very 
slightlf/ alkaline. The white of two eggs well beaten is now added, 
and the whole boiled vigorously for half an hour. It is tluMi tllterctl 
through a thick layer of sterilized t'otton into a tlask. and should 



136 VEGETABLE PARASITES. 

form a parfectly clear, slightly yellowish mass which is quite firm 
and solid on cooling. It is now filled into sterilized test tubes 
which have been plugged with cotton before sterilizing — about two 
inches in depth of the material being put into each tube — and these 
are steamed for from twenty minutes to half an hour, and again for 
an equal period on the f ollo^ving day, when they are ready for use 
(see Fig. 51 j. 

Xutrient Agar. — This is made and filled into tubes in the same 
way as the nutrient gelatin, save that one per cent of the agar is 
added in place of the gelatin. As the agar is less readily soluble 
than the gelatin, it Avill have to be boiled longer on the water bath 
before neutralizing. After the last sterihzation the agar tubes are 
placed in a slanting position to cool, so that the agar may present a 
long, obhque surface. 

The Beef Tea is made in the same wav, save that no sohdif^dno; 
material is added and it may be filtered through paper. 

The ILilk is prepared by filling it into test tubes (about the same 




Fig. 51.— a Gelatix Tube Culture. 
The bacterial gro-nth is confined to the seat of inoculation, i.e., the surface and the line of needle 
puncture below 

amount as in the case of gelatin) and steaming for an hour on two 
successive davs. 

The mode of preparing blood serum need not be considered here. 

Ha^-ing thus seen how the nutrient media are prepared, let us see 
briefly how they are used in studying the bacteria. 

In the first place, it is necessary to get from the various mixtures 
of several species, as they are apt to occur in nature or in diseased 
parts, single species growing by themselves, so that their hf e history 
and characters may be studied in detail. To show by an example 
how this is done, we will suppose that we have a sample of water 
containing^ bacteria, and Avish to learn how manv there are and of 
what species, and to get them into separate receptacles for study. 
We melt the gelatin in one of the test tubes, prepared as above de- 
scribed, which we know to contain no h^dng bacteria — because we 
have sterihzed both the tube and its contents by heat — and add to 
it a measured volume, usually 1 c.c, of the water, and mix them 
by gentle shaking ; we now take a glass plate, or a shallow covered 
glass dish cahed a Petri plate (see Fig. 53), which has been steril- 



VEGETABLE PARASITES. 



137 



ized by heat, lay it upon a cold surface, and pour out the mixture of 
water and nutrient gelatin in a thin layer upon it. When the 
gelatin solidifies, the invisible germs which the water contained are 
caught and held in position by it, and if the whole be now set away 
in a sufficiently warm place the living bacteria will presently com- 
mence to grow. 

After a few hours or days, from each one of the single living 
bacteria scattered through the gelatin so many new germs may have 
developed that they form a mass, called a colony, large enough to 
be visible to the naked eye. As different species grow in different 
ways, some forming colored colonies, some fluidifying the gelatin, 
some growing much more rapidly than others (see Fig. 52), we can 
usually recognize the different species either with the naked eye or 




Fig. 52.— a Gelatin Plate Culture of Drinking Water. 
Showing bacterial colonies of various species. This plate was made by mixing 1 c.c. of the 
ordinary drinking water of New York City with the nutrient gelatin, and allowing the bacteria 
to grow for two days. 

under the microscope, and with a fine, sterilized platinum needle can 
pick out portions of the different colonies and transfer them to the 
tubes of nutrient media of one land or another which we have pre- 
pared, and study their growth there in the form of pure cultures. 

The transfer of the germs to the tubes is made by plunging the 
needle which has touched the plate colonies down into the gelatin or 
agar, or drawing it over the surface of the potato. This is called 
inoculating the culture media. 

I^ot infrequently it is necessary to use the agar culture medium 
for plate cultures, because many disease-producing forms of germs 
do not grow at a temperature below that of the body, at which the 



138 



VEGETABLE PARASITES. 



gelatin fluidifies. In many cases, especially when we make agar 
plate cultures, we do not mi-x the material to be studied with the flu- 
idified culture medium and then let it cool, but we spread the mate- 
rial in Yevj thin streaks, with a sterilized platinum needle, over the 
surface of the already cooled nutrient film. Then setting the culture, 
carefully covered, in the incubator, we await the development of col- 
onies along the surface streaks (see Fig. 53). 

By the use of this principle of the plate culture, sometimes with 




Fig. 53.— Petri's Plate Cux^tuiie of Bacteria from the Mom'H. 
Made by streaking the surface of sterilized nutrient agar— previously poured into the shallow 
dish and cooled— with scrapings from tbe mouth, and allowing to stand in a warm place for forty- 
eight hours. The lighter spots are the ' ' colonies "'' or masses of germs of various forms which have 
grown from the invisible germs of the mouth. 

one form of culture medium, sometimes with another, and with va- 
rious modifications of the technique, we can separate the bacteria 
which occur in the body in disease, and, by combining animal inocu- 
lations with our other observations, can collect the data which en- 
able us to decide whether the bacteria which are associated with cer- 
tain lesions actually cause them. 



VEGETABLE PARASITES. 139 

The most scrupulous care is required in sterilizing the nutrient 
media and the utensils and instruments used, and the greatest cau- 
tion should be exercised, in transferring the bacteria from one re- 
ceptacle to another, to prevent contamination. A large experience in 
this sort of manipulation is necessary before reliable results can be 
obtained in original investigation, since the slightest error or care- 
lessness in manipulation, or failure to observe the occurrence of con- 
tamination, is liable to entirely vitiate the results of long series of ex- 
periments. It is only by an extended preliminary training in the 
cultivation of some of the more characteristic and easily recogniz- 
able forms, under a variety of conditions, in a perfectly pure state, 
through a series of generations, that one can be assured of his capa- 
city to carry on researches in this most difficult and intricate field. 

The methods of inoculation of animals with pure cultures, and 
the precautions to be observed, as well as a description of the vari- 
ous forms of apparatus made use of in practical bacteriology, must 
be sought in more extended treatises on this subject. 

It is wiser for one purposing to carry on bacterial researches to 
gain a practical acquaintance with methods and apparatus in a well- 
appointed laboratory, than to make the attempt to work out the meth- 
ods from books. 

Material obtained from the human body which is to be subjected 
to bacterial examination should be collected with every precaution 
against accidental contamination — if fluid, in steriHzed vessels ; if 
solid, wrapped in cloths saturated with 1 : 1,000 corrosive sublimate 
solution, and brought at the earliest possible moment to the labora- 
tory.' 

CLASSIFICATION OF BACTERIA. 

The systematic study of these organisms by exact and reliable 
methods is of such recent date, they are so small and difficult to ex- 
amine completely, and so much uncertainty still exists about the 

' The most complete treatise oa bacterial technology is Hueppes '' Methoden tier 
Bakterienf orsclmng. " 

As a laboratory manual for beginners Abbot'i^ " Principles of Bacteriology," 1802, 
is to be cordially recommended. 

i^ran^^rs *' Text Book of Bacteriology," translated by Linsley, 18^1 , presents a 
most admirable summary of the biology and technique. 

More extended works, such as Ban mgarf en's '"Lehrbuch der pathologischen 
Mykologie"; Maces " Traite pratique de Bacteriologie." 2d ed., 1892; Cornil und 
Babes' " Les Bacteries," 3d ed.; as Avell as the systematic list of described species in 
the " Bakteriologische Diagnostik,'' by Eisenberg, 3d ed., are quite indispensjibU^ 
for reference. 

But facts in this new field aro accunmhitiug so fast, and ]HMnts of view are so 
rapidly changing, that a large part of the record of detailed study is widely scat- 
tered in monographs and journals. 



140 VEGETABLE PARASITES. 

character and life history of many known forms, that a satisfactory 
and scientific classification of them is not jet possible. There are 
among them well-defined groups and wholly distinct genera and spe- 
cies which maintain their most marked characteristic morphological 
and biological features under all circumstances. Within certain 
limits, however, bacteria may undergo moderate variation in form 
and in metabolism. ^ 

The bacteria are often divided into two great groups depending 
upon the conditions under which they live. Those which nourish 
themselves on dead organic material are called saprophytes or sapro- 
phytic bacteria ; those which feed upon living organisms, parasites 
or parasitic bacteria. 

While some of the parasitic bacteria are always parasitic {obliga- 
tory parasites), there are others which are only occasionally para- 
sitic, being able to adapt themselves, within certain limits, to sur- 
rounding conditions ; these are called facultative parasites. There 
are others, furthermore, which usually are parasitic, but occasionally 
live as saprophytes ; these are facultative saprophytes. 

This classification is by no means an exact one, but it serves a 
useful purpose in indicating in a general way the favorite life condi- 
tions of different forms of bacteria. 

At present the most generally useful grouping of the bacteria is 
on a simple morphological basis. There are three primary groups : 

I. Spheroidal bacteria. 

II. Rod-shaped or filiform bacteria. 

III. Spiral-shaped bacteria.^ 

This classification or grouping of the bacteria is temporary and 
provisional, and, as our knowledge increases, will no doubt be 
essentially modified or altogether replaced ; but it is at present al- 
most indispensable for purposes of study. 

I. SPHEROIDAL BACTERIA (COCCI ' OR MICROCOCCI). 

The most common and important genus of this group of bacteria 
is Micrococcus, of which there are many species. Some of these are 
capable of producing coloring materials of various kinds in the nu- 
trient media ; others induce different forms of fermentation ; still 
others, occurring in the body in connection with various diseases, are 

1 When the bacteria are growing under unfavorable conditions, or when they are 
old or dead, they may assume various distorted, bizarre shapes, which are called 
iwDolution forms. 

^ In addition to these there are a few forms which present such variable shapes in 
different phases of their growth that they form a rather indefinite class by them- 
selves. 

^ Singular coccus, pronounced kok'-us ; plural cocci, pronounced kok'-si. 



VEGETABLE PARASITES. 141 

called pathogenic micrococci. The cells of most of the species 
of micrococci are very small, having, for the most part, a diameter 
of less than one-thousandth of a millimetre ;' but some forms are 
considerably larger. They occur either singly ; or in irregular clus- 
ters — staphylococci; or joined together in pairs — diplococci ; in 
longer or shorter beaded chains — streptococci; in tablet-like groups of 
four — merismopedia ; in packets or cubes of eight, or some multiple 
of eight — sarcince; or in zoogloea masses (see Figs. 54 and 56). But 
few of the micrococci exhibit spontaneous progressive movement, al- 






■•V-./ < 



I 



\) 



Fig. 54.— Spheroidal Bacteria (genus Micrococcus). 

1. Micrococcus from ulcerative endocarditis, a, single; 6, zoogloea. 

2. Micrococci cultivated from laboratory dust, a, in pairs (diplococcus form); &, io tetrads, 
M. tetragenus; c, in chains (streptococcus form). Stained with gentian violet. 

though, like small, light particles in general when suspended in fluids, 
they are liable to show the dancing tremor, called Brownian move- 
ment. Spore formation has not been observed in the members of this 




.^4 is#« 




Fig. 55.— Sarcin^. 
From a culture stained with gentian violet. Showing the growth form in cuboidal masses. 

group. The species differ from one another in size, sometimes slightly 
in shape, in mode of grouping, in retractile power, and in their physio- 
logical activities. But morphological characters do not suffice to 
characterize species. 

Saprophytic Cocci. 

A large number of cocci have been described and named, occur- 
ring in the soil, water, air, and upon the bodies of men and animals. 

Among the color-producing (chromogenic) micrococci m;iy be 
mentioned the Micrococcus luteas and Sarcina lutea, which are 
common in the dust of the air, and when growing in masses form 

' To express this (quantity the letter n is coiumoiily employed, 

12 



342 VEGETABLE PARASITES. 

yellow droplets on the surface of boiled potatoes or other nutrient 
media. 

The Micrococcus urece, which frequently occurs in urine, induces 
ammoniacal fermentation. Other species are found in fermenting 
wine and in a great variety of putrefying substances. 

Sarxina ventriculi is of not infrequent occurrence in the stomach 
of man under abnormal conditions. 

Micrococcus tetragenus (Fig. 54, 2&), which belongs in the group 

of Merismopedia, is of frequent occurrence in sputum and in lung 

cavities. 

Pathogenic Cocci. 

The characters of this group of bacteria and the lesions which 
they induce are considered in the section devoted to the Acute 
Infectious Diseases and in the part devoted to Special Organs. 




• * / 



/>/ 



f 1 

Fig. 56.— Bacilli in Pairs. 
1 was formerly called Bacterium termo, and 2, B. lineola. 

II. ROD-SHAPED OR FILIFORM BACTERIA. 

The most common and important genus in this group is called 
Bacillus. Some of the bacilli are short and are apt to be grouped 
in pairs (seo Fig. 56). 





Fio. 57. Fig. 58. 

Fig. 57.— Bacilli arranged End to End, forming Chains. 

Cultivated from laboratory air. 

Fig. 58.— Curved Bacilli, forming Spiral Chains. 
Spirillum tyrogenum. 

Some are long and may form chains or threads (see Fig. 57) ; 
some are slightly curved, and when joined together end to end, as is 
apt to occur in their growth, they form spirals (Fig. b^). 

Some of the bacilli are immobile ; others are capable of perform- 
ing the most varied movements when suspended in fluids. Many of 
the bacilli are concerned in the ordinary processes of decay which we 
call putrefaction, and are entirely harmless when introduced into the 



Q 



VEGETABLE PARASITES. 14.: 

human or animal body. Many produce brilliant colors, red, yellow, 
green, etc. , when growing in large masses. 

Saprophytic Bacilli, 

Of this large group only the following need be mentioned : 

The Bacillus acicli lactici is very wide-sj)read, and by its meta- 
bolism lactose is converted into lactic acid. 

Bacillus pyocyaiiiis is of occasional occurrence in wounds, de- 
veloping a greenish-blue color on the bandages. 

Bacillus prod igiosiis develops a brilliant blood-red color in spots 
and masses on the culture media. 

Proteus vulgaris is an extremely common species of bacillus in 
putrefying organic substances. 

Leptothrix. — There exist under almost all conditions in the 
mouth and about the junction of the teeth and gums^ single or in 
larger or smaller masses, long, slender, filiform bacilli, usually with- 
out transverse divisions, which have received the general name 




Fig. 59.— Leptothrix buccalis with Micrococcus Colonies. 
From the mouth of a healthy person. 

Leptothrix huccalis. There are some reasons for supposing that 
they may be concerned in caries of the teeth, in connection with 
which they are often found. But, beyond this fairly well-founded 
conjecture, we have no reason to suspect them to be of any patho- 
genic significance. They are frequently entangled among scattered 
or larger and smaller masses of micococci (Fig. 59). Leptothrix is a 
general name only, and we do not know whether it represents a sin- 
gle genus or species, or wliether it is made up of undeveloped forms 
of some varieties of bacillus. 

Bacillns coli communis is a species always present in the intes- 
tinal canal of man, which may, under favoring conditions, enter the 
body and become disease-producing. 

Pathogen ic Bacilli. 

Certain bacilli not ordinarily found in the body are capable, ^vhou 
they gain access to it, of inducing serious disease, and even death — 
pathogenic bacilli. Thus malignant pustule, tuberculosis, typhoid 
[ever, leprosy, glanders, diphtheria, tetanus, rhinoscleroma, and 



144 VEGETABLE PARASITES. 

other infectious diseases, have been proven to be caused hj different 
species of bacilli, which will be considered later in this book under 
their appropriate headings. 

III. SPIRAL-SHAPED BACTERIA. 

The spirals of these cells may be closed or open, few in number 
or numerous ; some of them are ciliated at the ends. 

Saprophytic Spirilla. 

One of the most common genera in this group is Spirillum. 
Spirillum rugula occurs in swamp water, on the surfaces of the 
teeth, and in faeces. It is thick, has open spirals, and occurs in 
chains or interlacing masses. Other species, among which may be 
mentioned S. serpens (Fig. 60), occur in stagnant water and in pu- 
trefying fluids. 





Fig. 60. Fig. 61. 

Fig. 60.— Spirillum serpens. 

From putrefying hay infusion. 

Fig. 61.— Spirochete denticola. 
From mouth of healthy person. 

An interesting species of spirillum, called Spirillum ruhriim, de- 
velops ingrowing a rich red color, differing from many color forming 
bacteria in the fact that the color is developed best out of free contact 
with the air. 

Another important genus of spiro-bacteria is Spirochcete, whose 
cells are in general larger and more flexible than those of spirillum, 
with more closely set spirals. 

Spirochcete denticola is found in the mucous membrane of the 
mouth and on the teeth mixed with lei3tothrix, and also in carious 
teeth. It is usualh' about 10 to 20 }.i long, and pointed at the ends 
(Fig. 61). S. j)licatilis is about 110 to 225 /i long, very slender, 
^vith many spirals, and blunt ends. It moves ^vith great rapidity, 
and is frequently found in summer in swamp water and in eave- 
troughs. 

Pathogenic Spirilla. 

These are few in number and will be considered among the infec- 
tious diseases. 



VEGETABLE PARASITES. 



145 



II. YEASTS. 

These micro-organisms consist of oval or spheroidal cells with 
granular protoplasm and a thin membrane. They multiply by 
sprouts or buds from the parent cell. The new individuals may 
separate from the old, or may cling to them so that chain-like combina- 



FiG. 62.— Yeast— Saccharomyces. 

tions may occur (Fig. 62). Some species of yeast set up fermen- 
tation in fluids containing sugar. They may grow to a certain ex- 
tent in the stomach and in the bladder in diabetes, but appear to be 
of little importance in human pathology. 




Fig. 63.— x^spergillus glaucus. 
Showing mycelium, from which arise the spore-bearing stmctm-es. 



III. MOULDS. 

The moulds are considerably more complex in structure than 
either the bacteria or tlie veasts. Some of the forms are verv com- 
mon and universall}- known. In general, it may be said that the 
moulds consist of a series of delicate, translucent, jointed threads — 
mycelium — from which, either directly or through the intervention 
of a special structure, the sporangium, the spores are developed 



146 



VEGETABLE PARASITES. 



(Fig. G3). The moulds which are apt to occur in the human body may 
be of the former, more simple, or of the latter, more complex type. 

Among the simpler forms of moulds which occur in the body 
may be mentioned the Achorion Schonleinii, Microsporon furfur. 
Trichophyton tonsurans. There is a close morphological resemblance 
between these forms. 

Achorion Schdnleinii, the favus fungus, is formed of a much- 
branching mycelium from which the spores are directly developed 
(Fig. 64). It grows readily on artificial culture media, such as nu- 
trient agar and gelatin, at the temperature of the body. This fun- 
gus is most apt to grow upon the hairy part of the head, where it 
forms small surface crusts and grows into the shafts and root 
sheaths of the hair, exciting inflammation in the adjacent tissue. 

Trichophyton tonsurans develops in the form of a moderately 
branching mycelium, forming comparatively few spores. It grows 




Fig. 64.— Achorion Schoxleixii— Favts. 
From a culture. 



in the skin, either about or apart from the hairs, or in the nails, pro- 
ducing the lesions of various phases of herpes, which differ consid- 
erably, depending upon the particular structures involved. At body 
temperature it grows readily on artificial culture media, differing 
markedly in appearance from achorion, to which it is morphologi- 
cally quite similar. 

Microsporon furfur, the mould fungus causing pityriasis ver- 
sicolor, is more prone than the achorion to the development of many 
spores, but otherwise considerably resembles it morphologically. 
It has not yet been cultivated on artificial media. By its infil- 
tration of the epidermis, especially of the body and upper extremi- 
ties, it causes larger and smaller yello^vish or brownish patches. 

The more complex types of moulds are only occasional dwellers 
in the human body and appear to be but rarely the cause of disease, 



VEGETABLE PARASITES. l47 

passing rather a sai^ropliytic existence on dead material in parts of 
the body which are in communication with the air. Thus they may 
be found growing on accumulations in the external auditory canal, 
in dead tissues in the lungs, on walls of cavities, dilated bronchi, 
etc. 

A lowly form of micro-organism frequently found growing in the 
mouth and fauces and oesophagus of children, in the form of a whit- 
ish pellicle, is the so-called Oidium albicans, which consists of 
branching, jointed threads and spores which penetrate between the 
epithelial cells. This fungus may assume considerable importance, 
when in very feeble children it blocks the oesophagus, or when, as 
is rarely the case, from the surface of ulcers it penetrates the blood 
vessels and gives rise to visceral metastasis. The exact relationship 
of this fungus to the moulds is not yet very clear. 

METHODS OF STUDYING YEASTS AND MOULDS. 

The yeast organisms are in general stained and cultivated by the 
same methods as those used in studying the bacteria. The moulds 
may be simply teased and studied in glycerin or in glycerin and wa- 
ter. They may be stained with dilute aqueous fuchsin solution or 
with alkalin-methyl-blue solution (Loffler's solution, see page 133). 
When spores have formed in considerable numbers on the more com- 
plex forms of moulds, they are not easily wetted by the usual stain- 
ing fluids, because the air clings so closely among the spore masses. 
In a mixture of four parts of alcohol and one of aqueous solution of 
ammonia they are instantly wetted, and may then, with or without 
staining, be teased and mounted in glycerin. In studying the fun- 
gous masses in the above-described skin diseases it is well, when 
crust-like masses are to be teased apart, to allow them flrst to soak 
for a few moments in five-per-cent solution of caustic potash. In 
this solution they may be studied, or they may be teased and mounted 
in glycerin for preservation. Most of the more common moulds are 
readily grown on the ordinary culture media. 



THE INFECTIOUS DISEASES." 



Infectious diseases are those caused by the entrance into the 
body and proUferation there of pathogenic micro-organisms. 

An infectious disease is contagious when the micro-organism 
which incites it (the contagium) can, under the ordinary conditions 
of Hfe, be conveyed from the sick to the well in a condition to set up 
the disease anew. 

^ For more detailed consideration of tlie themes considered in this section, with 
reference to bibliography, the reader may consult Bailing arten' s "Lehrbuch der 
pathologischen Mykologie," and Ziegler's " Lehrbuch der pathologischen Ana- 
tomic," Bd. i., 7th ed., 1892. 

For later and current researches one shoald consult the files of Baumgarten^'s 
" Jahresbericht iiber die Fortschritte in der Lehre von den pathogenen Mikroorgan- 
ism.en"' ; the Centralblatt fiir Bakteriologie ; the Index Medicus, and the various 
special journals devoted to pathology and bacteriology. 



INFECTIOUS DISEASES INDUCED BY THE PYOGENIC 

BACTERIA. 

There is a considerable number of very important inflammatory 
lesions, closely allied in their character, and commonly, though not 
always, associated with suppuration, which are due to the presence 
and growth in the body of the spheroidal bacteria or cocci known 
as Staphylococcus pyogenes and Streptococcus pyogenes. While 
other micro-organisms may induce suppuration, these are to be con- 
sidered as par excellence the pyogenic bacteria. 

We will first consider the morphological and biological charac- 
ters of these germs and their relation to suppurative inflammation, 
and then, in order, the other special forms of disease with which 
they are associated. 







Fig. 65.— Staphylococcus pyogenes aureus. 
From a beef-tea culture. Stained with gentian violet. 

The staphylococcus pyogenes cmreus (Fig. 65) is in general a 
small coccus, the individuals varying, however, considerably in size. 
In its growth it does not show a characteristic grouping, but grows 
in irregular masses and heaps (the somewhat crude resemblance to a 
bunch of grapes gave rise to the generic name) ; sometimes, how- 
ever, pairs and groups of four or short rows of the cocci are seen. 
The germ is readily stained by the anilin dyes, and does not lose its 
color in Grain's method of staining. It does not show spontaneous 
movement, and, like other spheroidal forms, does not appear to devel- 
op spores. It is quite tenacious of vitality, surviving long drying 
and degrees of heat and cold and an exposure to chemical bacteri- 
cides to whic^h many pathogenic germs readily succumb. It grows 
well at ordinary room temperature in such artificial culture media 
as nutrient gelatin, agar, beef tea, and milk, and mi potatoes, forming 
somewhat voluminous masses of culiinv. It rapidly fluiditii^s gela- 



150 THE INFECTIOUS DISEASES. 

tin, and in the various media develops a yellowish- white or a deep 
golden-yellow color, whence its specific name, aureus, and its com- 
mon name, ''golden coccus/' The virulence of cultures obtained 
from different sources varies a good deal, but in general suppura- 
tion is apt to follow its subcutaneous injection into rabbits, mice, 
and guinea-pigs. Injection into the ear vein of the rabbit is usually 
followed by multiple abscesses in the kidney, suppuration of joints, 
etc. 

In man this coccus grows readily and rapidly, and may cause 
necrosis and exudative inflammation, especially in its suppurative 
phases (Fig. 66). The lesions which it induces are apt to be circum- 
scribed. It may cause pustules, boils, and abscesses, and various 







Fig. 66. — Staphylococcus pyogenes aureus, in and among the Pus Cells in an Abscess of 

THE Kidney. 

suppurative inflammations of the viscera and serous membranes, 
joints, bones, endocardium, etc. These effects may be induced by 
the staphylococcus alone or by it in associa^tion with other species 
of germs. Its relationship to pyaemia will be considered under that 
heading. 

The Staphylococcus pyogenes aureus apparently produces its 
effects in the body in virtue of certain toxins or toxalbumins 
Avhich are produced as the result of its metabolism, and which are 
either at once set free or stored up in the body of the germs 
until their release by disintegration after the death of the germs. 
The special power of the staphjdococcus to cause the gathering of 
leucocytes is doubtless due to the marked chemotactic powers of 



THE INFECTIOUS DISEASES. loi 

some of the proteid substances in its protoplasm (see page 120). But 
here, as with other pathogenic germs, we shall do well not to be to(j 
precise in assigning closely the minute phases of lesions to definite 
chemical products of germ metabolism ; because these are very com- 
plex indeed, and our field of observation on them but newly opened. 
'Nov is our knowledge of the particular element in the germ or its 
products which is prone to induce necrosis at all precise. 

The Staphylococcus pyogenes may obtain entrance to the body 
through wounds, small or large, of the skin or mucous membranes. 
The possibility of its entrance through uninjured surfaces has been 
demonstrated. In many cases we are quite unable to trace its 
mode of access. While in the natural course of events this germ 
tends to die off in the body, it may yet remain for a long time alive. 

It is widespread in inhabited regions, especially in towns, being 
frequently found on the surface of the body, and in the saliva, es- 
pecially of those with acute or chronic catarrh of the upper air 
passages. As the result of the filthy habit of indiscriminate pubhc 
spitting, it is common in the dust of hospitals, houses, towns, and 
places of public assembly. 

Staphylococcus pyogenes albus. — This appears to be a variety of 
the Staphylococcus pyogenes aureus which does not develop the yel- 
low color in cultures. It is of frequent occurrence both in connec- 
tion with the aureus and alone. Its action on the body is similar, 
but it has seemed to many observers to be in general less virulent. 

Staphylococcus epidermidis albus. — This coccus has been de- 
scribed by Welch ^ as of frequent occurrence in the epidermis, and 
although of rather feeble pyogenic power, yet seems frequently to 
cause small stitch abscess and moderate suppuration along drainage 
tubes. Welch regards it as possibly a variety of Staphylococcus 
pyogenes albus. 

Streptococcus pyogenes. — This coccus is distinguished morpho- 
logically from those just described by the marked tendency which 
the individuals exhibit, when growing, to hang together in longer or 
shorter chains (Fig. 67). It is in general rather larger than the Sta- 
phylococcus pyogenes aureus ; is, like it, immobile, and stains easily 
in the same way. 

It grows readily, but more slowly than the staphylococcus, on the 
ordinary culture media. It does not fluidity gelatin, on which it 
grows as small, inconspicuous, graj'ish-Avhite colonies. On the sur- 
face of agar plates kept in the thermostat at 37° C. for twenty-four 
hours, the small grayish colonies usually show under the microscope 



^ Welch, " Wound Infectiou,'' Americau Journal of the ^ledieal Sciences, vol. 
p. 457, 1891. 



153 THE INFECTIOUS DISEASES. 

loops and fringes of the chain-like cocci extending off from the bor- 
ders. The growth on potatoes is inconspicuous. In beef tea it 
usually forms delicate, flocculent masses, which cling to the sides of 
the tubes, lea^dng the fluid clear. It coagulates milk when in vigor- 
ous growth. 

The results of animal inoculation with the Streptococcus pyogenes 
are in general similar to those ^vith the Staphylococcus pyogenes 
aureus, but its effects are rather less marked and its action more un- 
certain. The streptococcus is very frequently associated with Sta- 
phylococcus pyogenes aureus both in its distribution outside the body, 
in healthy persons, and in disease. In general it may be said that the 
streptococcus incites those forms of suppuration and fibro-purulent 
inflammation which tend to spread both locally and through meta- 
stasis. 

We may summarize the prominent local effects of the pyogenic 
bacteria in the body by saying that they tend to induce the gather- 






Fig. 67. — Streptococcus pyogenes. From a beef -tea culture. 

ing of leucocytes by chemotaxis, they stimulate cell proliferation, 
and they are prone to induce tissue necrosis. 

Other forms of bacteria than the pyogenic cocci may incite sup- 
purative inflammation. Thus the pneumococcus, the typhoid bacil- 
lus, and the tubercle bacillus not infrequently, in addition to their 
more common and characteristic action in the body, set up complicat- 
ing suppurations. Several other forms of germs have been found 
in suppurative inflammation, which we need only mention here : 
Staphylococcus gilvus ; Staphylococcus pyogenes citreus ; Staphylo- 
coccus salivarius pyogenes ; Staphylococcus cereus albus and flavus ; 
Micrococcus tetragenus ; Bacillus coli communis ; Bacillus pyogenes 
foetidus ; and Bacillus pyocyanus. Bolton has recently described a 
pyogenic bacillus occurring in the soil — Bacillus pyogenes soli. ^ 

The bacteria which are found in the various phases of suppurative 
inflammation ma}' lie free in the interstices of the tissue with the 
exudate, or they may be in part within the cells which have gath- 
ered (see Fig. GG). 

* Bolton, American Journal of the Medical Sciences, June, 1892, 



ERYSIPELAS. 

Erysipelas is a diffuse inflammation of the skin and subcutaneous 
tissue which tends to spread, and which especially involves the lymph 
spaces and the lymph vessels. It is characterized locally by swelling 
of the tissue and a bright red color of the integument. It is regularly 
accompanied by constitutional disturbances, the most marked of which 
is fever. The morphological changes at the seat of lesion, as we see 
them after death, vary considerably in different cases and in different 
stages of the disease. The redness of the disease usually disappears 
after death. But the tissues may be swollen b}^ the accumulation of 
serous fluid. This fluid may be nearly transparent, or turbid from 
















• ♦, , : .-s^sg^ssSiceS 



^tp^^ ■ . ■.^••*VV... V- -""■^""'.- ^ "■■-■ - "■ ■': .:r--''<^^^''^^' 

--.,^/ '■'■.■•■» ^ _ — • ;..,.^', ■ """' .■■■.."—■ "■"■■'" — ^^r "" 

ITiG. 68.— Erysipelas of the Skin. 
Showing streptococci in the lymph spaces. 




admixture with pus cells. Pus cells may infiltrate the tissues either 
sparsely or in dense masses. Sometimes vesicles are found on the 
surface, or scabs ; sometimes more or less of the aft'ected region be- 
comes filled with abscesses or gangrenous. In some cases we find, 
aside from the local lesions, petechiiB in the serous membranes, swell- 
ing of the spleen, and parenchymatous degeneration of tlie kidneys 
and liver. 

The researches of Fehleisen and others have shown that erysipelas 
is caused by the presence and action in the tissues of a. chain coccus 
(Fig. GS) called Streptococcus enjsipelatis. These bacteria arc 
usually most abundant in the lymph vessels and lymph spaces along 



154 



THE INFECTIOUS DISEASES. 



the advancing borders of the inflamniatory area, but they may be 
contained in the blood vessels (see Fig. 69). 

In its morphological and biological characters the so-called Strep- 
tococcus erysipelatis appears to be identical Tvith the Streptococcus 
pyogenes. 

Inoculation of rabbits Tvith the pure culture may induce a fairly 
typical erysipelatous inflammation, but, as these animals are not espe- 
cially susceptible to its action, the results of inoculations are not con- 
stant. 

There appears to be much reason for belie^T.ng that many forms of 




Fig. 69.— Streptococci in Masses in the Blood axd Ltjiph Vessels of the Skin in Erysipelas. 



phlegmonous and other exudative inflammation, and many forms of 
erysipelas, are different phases of the inflammatory process due to 
the same organism; the difference in the reaction of the tissues which 
constitute the chnical differences characteristic of the different dis- 
eases being due, perhaps to differences in the tissues involved, per- 
haps to variations in the characters and virulence of the germ, and 
perhaps to causes which at present we know nothing about. 

Further researches are required to fully explain the exact relation- 
ship of these at least closely allied forms of inflammation to one an- 
other and to the bacteria which cause them. 



ACUTE CEREBRO-SPINAL MENKsTGITIS. 

This is an acute infectious disease, characterized by an exudative 
inflammation of the pia mater of the brain and spinal cord. The de- 
gree of the lesion in the meninges varies greatly, depending upon 
the period at which death occurs. In some cases, when death occurs 
early in the disease, there may be to the naked eye no evident change 
in the membranes, or a moderate serous infiltration. In these cases 
the microscope may reveal a moderate degree of extravasation of 
leucocytes in the vicinity of the vessels. In the well-marked cases 
the pia mater of the brain and cord is more or less densely infiltrat- 
ed with serum, fibrin, and pus. This may occur over the convex- 
ity and base of the brain, and is frequently most marked in the 
latter situation. In the cord the infiltration may occur over the ante- 
rior and posterior surfaces, but in many cases, probably owing to 
the recumbent position of the patient, it is most marked on the pos- 
terior surface. The ventricles of the brain and the central canal of 
the cord may contain turbid serum mingled with pus cells, and 
sometimes blood cells. The membranes and underlying nerve tissue 
may be hyper^emic and the seat of capillary haemorrhages. Rarely 
a small amount of pus and fibrin may be found between the pia and 
dura mater. 

In protracted cases the ventricles may be dilated with serum and 
the exudation in the meninges may become fatty or dense and 
cheesy. 

While the above are the characteristic lesions of this disease, 
there are a number of secondary clianges in different parts of the 
body which are not constant, but which occur with sufficient fre- 
quency to render their mention necessary. There may be subserous 
punctate haemorrhages in the endocardium ; petechiiie in the skin : liy- 
alin and granular degeneration in the voluntary striated muscle: 
occasional multiple abscesses in various parts of the body ; suppura- 
tive inflammation of the joints ; parenchymatous degeiieratitni of the 
heart, liver, and kidneys ; and swelling of the gastro-intestinal lym- 
phatic apparatus. 

Cerebro-spinal meningitis may occur by itself or in connection 
with some other acute infectious disease, such as acute lobar puou- 



156 THE INFECTIOUS DISEASES. 

monia, mycotic ulcerative endocarditis, pysemia, multiple suppura- 
tive arthritis, otitis media, puerperal fever, typhoid fever, etc. 

The lesions are essentially the same in epidemic and in sporadic 
cases of acute cerebro- spinal meningitis, and there is much reason 
to believe that in both modes of occurrence the disease is caused by 
bacteria. But sufficient studies of the epidemic form of the disease 
have not yet been made by the new methods, so that we cannot 
say much which is definite about its causation. 

On the other hand, numerous careful studies have been made on 
the bacteria occurring at the seat of lesion in sporadic cases occur- 
ring both with and without complicating lesions in other parts of the 
bodv. 

The StreptocoGCiis pyogenes has been demonstrated in a few 
cases, occurring in connection with suppurative inflammations else- 
where. 

The Pneumococcus of Frdnkel (see page 162) has been found in 
several cases, and in some of these without any lung lesion. Weich- 
selbaum has described the occurrence in several cases of a diplo- 
coccus not known to occur elsewhere, which was found largely con- 
fined to the pus cells, and which he called Diplococcus intracellu- 
laris meningitidis. Animal experiments ^vith this as well as the 
pneumococcus would indicate that they stand in a causative relation 
to the disease. Some other scattering forms of bacteria have been 
described, but not with sufficient frequency and definitiveness to 
enable us to judge of their significance. 

It seems probable, therefore, from what we know at present, 
that several forms of bacteria are capable of causing acute cerebro- 
spinal meningitis. Which is the most frequent and important it re- 
mains for further researches to show.^ 

^ For literature and further details consult Weichselbaum, Fortschritte der Mediciu, 
September loth, 1887 ; Goldschmidi , Centralblatt flir Bakteriologie, Bd. ii., No. 22, 
X^^l ', Neumann and Schaefer, Virchow's Archiv, Bd. cix., p. 477. 



PY JEMI A . AND SEPTICEMIA. 

It has long been known that a certain number of persons who 
have received wounds by accident or by the hands of the surgeon 
may suffer from constitutional symptoms and develop lesions. To 
designate the condition of these patients the terms pysemia, septi- 
caemia, septico-pysemia, ichorsemia, inflammatory fever, surgical 
fever, traumatic fever, suppurative fever, and purulent infection 
have been used. Attempts have been made to distinguish several 
different forms of disease, and to call one pyaemia, another septicae- 
mia, and so on ; but these attempts have not hitherto proved very 
satisfactory, because the cause and nature of the various conditions 
were not definitely understood. 

Since, however, we have come to know that all these protean 
phases of allied disease are usually directly or indirectly dependent 
upon the growth of micro-organisms of one kind or another, we are 
able to make at least a general distinction between two fairly typical 
phases. 

If from a focus of suppurative inflammation due to the pyogenic 
or other bacteria, or if from a point of entrance of the pyogenic or 
other bacteria without local reaction, the germs or their products be- 
come distributed by metastasis, so that, with fever, embolic inflam- 
matory or suppurative foci are established, the condition is called 
pycemia. This condition, in the larger proportion of cases, is in- 
duced by the distribution of the Staphylococcus pyogenes or the 
Streptococcus pyogenes, or both. 

When, on the other hand, the body at large becomes poisoned by 
the absorption of toxic substances, such as toxins, toxalbiimins, or 
other products of bacterial metabolism, but without the development of 
metastatic suppurative foci, the condition is called sepficcenn'a: the 
fundamental difference in the conception of the two conditions being 
that septiciiemia is a general septic intoxication without lesions which 
show the distribution of micro-organisms through the blood or lymph, 
while in pyaemia such a distribution has occurred and secondary in- 
flammatory foci have been established. 

Very frequently, indeed, both conditions are associated, and thou 
the term septico-pycBuiia or pyo-septicimnia may be a}>propriate and 
usefid. 

U 



158 



THE INFECTIOUS DISEASES. 



While pyeemia and septicsemia in all their varied and coniinin<^- 
ling phases are very frequently due to the presence and growth in the 
body of the Staphylococcus pyogenes and the Streptococcus pyogenes, 
it should be borne in mind that other germs may induce these condi- 
tions, and that from the beginning the seat of growth and medium of 
distribution may be the blood itself. It should also be remembered 
that the point of introduction into the body of the offending germs 
'may be wholly concealed and not associated with any form of de- 
monstrable external lesion. This is often called cryptogenetic pyae- 
mia or septico-pysemia. Finally, the possibility should not be lost 
sight of that, under certain little understood conditions, toxic materials 
may be elaborated by the body cells themselves, which may give rise 
to st)me of the phenomena of septic poisoning. 




Fig. 70.— Micrococci in Masses in the Fibrinous Exudation of Pyemic Pleurisy. 

The varying phases of so-called piterpera//ei'^r are to be classed 
under the heading of septicsemia or pyaemia. 

After death from septicaemia and pyaemia there is a considerable 
variety in the post-mortem appearances. 

1. There are cases in which there are no recognizable lesions. 

2. There are cases characterized by early post-mortem decomposi- 
tion ; post-mortem staining of the tissues ; congestion of the lungs, 
stomach, intestines, and kidneys ; extravasations of blood in the 
serous membranes ; swelling of the solitary and agminated lymph 
nodules in the small intestine ; swelling of the spleen and parenchy- 
matous degeneration of the liver and kidneys. 

3. In some cases there are localized inflammations. The joints, 
the connective tissue around the joints, the pleura (Figs. 49 and 70), 



THE INFECTIOUS DISEASES. 150 

the pericardium, the peritoneum, the pia mater, and the connective 
tissue in different parts of the body may be inflamed. These local 
inflammations are of a purulent character, except in the serous mem- 
branes, where the principal inflammatory product may be fibrin. 

4. There are cases in which the veins in the neighborhood of the 
wound contain softened, puriform thrombi ; there are no infarc- 
tions in the viscera, but there may be inflammation of the joints and 
serous membranes. 

5. In other cases the veins contain thrombi ; there are infarctions 
and abscesses in the viscera ; local inflammations of the joints and 
serous membranes may be present or absent. The thrombi are 
formed regularly in the veins near the wound, but they may be 
situated in veins at a distance, and sometimes, although infarctions 
and abscesses are present, no thrombus can be discovered. The veins 
may be distended by the thrombi or only contain small coagula. 
The different kinds of thrombi, and the varieties of emboli and infarc- 
tions which they produce, are described in the article on Thrombosis, 
page 59. 



INFECTIOUS PSEUDO-MEMBRAN^OUS mFLAMMATION 

OF MUCOUS MEMBRATnTES. 

{Infectious Croupous Inflammation.) 

Under a variety of conditions, as during scarlatina and measles, 
or entirely apart from any complicating disorder, an acute exudative 
inflammation of the mucous membranes, especially of the upper air 
passages, occurs, which is regularly associated with, and is apparent- 
ly caused by, the growth of a streptococcus (Figs. 71 and 72) which 
in morphological and biological characters seems to be identical with 




Fig. 71.— Infectious Croupous Inflammation of the Trachea. 
Section through the pseudo-membrane and underlying tissue, showing large numbers of strep- 
tococci. 

the Streptococcus pyogenes and Streptococcus erysipelatis. There 
may be much or little fibrinous exudate ; there may in early stages, 
or even throughout, be none at all. The pellicle when formed may 
be loose or adherent, sharply circumscribed or tending to spread. 
The submucous tissue may show little change, or may be congested 
and oedematous, or may be the seat of suppurative inflammation 
(see Fig\ 24). The process may be confined to the tonsils. While 
under these varjdng conditions the inflammatory process is usually 
a localone and runs its course with or without the spnptoms of sep- 



THE INFECTIOUS DISEASES. 101 

ticsemia, occasionally the streptococcus finds access to the blood and 
may induce the lesions of pyaemia. On the other hand, it may by 
aspiration gain access to the lungs and induce varying phases of com- 
plicating broncho-pneumonia. The Staphylococcus pyogenes is not 
infrequently associated with the streptococcus in these lesions, but is 
not apparently of primary significance. Simulating very closely, as 
it does in many cases, both the local and general phenomena of diph- 
theria, this disorder has formerly been confounded with it, and is 
only recently recognized as a distinct phase of disease. It is now 




Fig. 72.— Streptococcus of Croupous Inflammation. 
From a beef-tea culture. 

frequently called pseudo-diphtheria. It seems in part to cover the 
condition formerly known as croup, in part those cases formerly 
thought to be mild diphtheria.' In many phases of acute angina, 
in many cases of follicular tonsillitis, streptococci have been found 
in large numbers. 



^ For a general consideration of the relationsliip between this form of pseudo- 
membranous inflammation and diphtheria, with original studies and bibliography, 
consult Park, " Diphtheria and Allied Pseudo-membranous Inflammations," Medical 
Record, July 30th and August 6th, 1892. 



INFECTIOUS DISEASES INDUCED BY THE 
DIPLOCOCCUS PNEUMOXIJE. 

{Pneumococciis ; Diplococcus Laiiceolatus.) 

This germ is commonly spoken of as the pneumococcus of Frankel, 
because its significance and hf e history in connection with acute lobar 
pneumonia were first demonstrated by him. ^ During their develop- 
ment these germs are distinctly spheroidal. But in their mature con- 
dition they are apt to become slightly elongated and often a little 
broader at one end than at the other, assuming a lanceolate form. 
They are very apt to occur in pairs, and frequently are seen in short 
chains, rarely in long chains. Very frequently, when gromng in 
the living animal, the pneumococcus is surrounded by a distinct, 
homogeneous capsule of varjdng thickness (see Fig. 73). This 

Fig. 73.— DiPLococcas Pneumonle (E^eumococcus). 
From a case of empyeema following lobar pneumonia ; showing lanceolate forms and. capsule. 

capsule does not, as a rule, develop in artificial cultures. The coccus 
itself is readily stained ; the capsule with difficulty. 

The pneumococcus has no spontaneous movement and grows but 
feebly at ordinary room temperature. It grows much better at the 
temperature of the body, forming on the surface of very slightly 
alkaline agar plates faint grayish, dewdrop-like, inconspicuous colo- 
nies, somewhat similar to those of Streptococcus pyogenes, but usu- 
ally more delicate. In beef tea it forms at body temperature a faint 
whitish sediment with slight turbidity of the fluid. As a rule, the 
cultures are prone to soon lose their ^drulence and to die off early. 
The pneumococcus injected, while virulent, subcutaneously into mice 

' It was discovered by Sternberg in saliva, and its pathogenic power demonstrated, 
some years before its full significance was understood in connection with pneumonia. 



THE INFECTIOUS DISEASES. 163 

and rabbits induces a rapidly fatal septicaemia, often with little marked 
anatomical change, save enlargement of the spleen. Sometimes 
there are necrotic foci in the liver, fibrin in the glomeruli of the kid- 
neys, fatty degeneration of the heart. Suppurative inflammation at 
the seat of inoculation and elsewhere may follow. The blood and 
viscera may show under these conditions numerous cocci, mostly ^vith 
capsules, or they may be confined to the seat of inoculation. Cul- 
tures which have been reduced in virulence, so as not to cause early 
death by septicaemia, may, when introduced into the trachea of rab- 
bits, induce a fairly typical lobar pneumonia. 

Different species of animals show marked differences in vulner- 
ability to the ravages of the pneumococcus. This germ is the most 
frequent and probably the exclusive inciter of acute lobar pneumonia 
in man. It appears to act, in part at least, by the development of an 
albuminous poison which has been tentatively called pneumotoxin. 
It would seem to be the pneumotoxin which induces the symptoms in 
acute lobar pneumonia indicative oi systemic poisoning, since the 
bacteria thems(3lves are usually confined to the lungs. ' 

For a more detailed description of these lesions of pneumonia, 
and an account of other bacteria which may be present, see page 
359. In addition to its more common effect in inducing lobar 
pneumonia, this diplococcus has been very frequently found in, and 
stands apparently in a causative relation to, some forms of exudative 
inflammation of the serous membranes, either in connection with 
or without a primary lobar pneumonia. Thus, it has been repeatedly 
found in otitis, meningitis, empysema, pericarditis, endocarditis, and 
in peritonitis. It has also been found in abscesses of the viscera and 
in exudative inflammation of the joints. The Diplococcus pneumoniae 
appears to be a frequent inhabitant of the mouth, even in health. It 
has been found in the mouths of about twenty per cent of healthy 
persons examined. It is thrown off in the sputum in lobar pneumo- 
nia, and no doubt from these sources in the dried condition, as dust, 
affords the contagium which in favoring conditions of the body 
lights up the inflammatory process in the lungs. 

To stain the pneumococcus with the capsule one should prepare 
the exudate containing it, or the sputum, on a cover glass in the man- 
ner described on page 1G3. This is then stained with anilin-gentian- 
violet solution (see page 132) for five minutes. Then one rinses rapidly 
with alcohol and washes this quickly off with water, in which the 
specimen is best studied. But it may be dried and mounted in bal- 

' Recent experimeuts have seemed to indicate that at a certain period of tlie disease 
the blood or body juices are capable of developing a substance antidotal to this pneu- 
motoxin, the advent of the former being signalized bv the so-called "crisis." 



164 THE INFECTIOUS DISEASES. 

sam. The color of the capsule is often faint. The pneumococcus 
may be stained in sections with Lofflers methyl- blue solution (page 
133) or by Weigert's modification of Gram's method with preliminar}' 
contrast stain (see page 132). By the latter method the fibrin in the 
pneiunonic exudate may be also stained. 



GOI^ORRHCEA 

AND OTHER INFLAMMATORY LESIONS INDUCED BY THE MICRO- 
COCCUS GONORRHOEA (GONOCOCCUS). 

The Micrococcus gonorrhoeae is most commonly found in the exu- 
date of gonorrhoeal inflammation of the mucous membranes. It 
may be also found free or enclosed in leucocytes within or between 
the superficial epithelial cells. It is also of frequent occurrence in 
the exudate in arthritis, and tubal, ovarian, perimetritic, and other 
inflammations, occurring as complications of gonorrhoea. 

Under these complicating conditions the gonococcus may occur 
alone or in association with the pyogenic cocci. It is generally most 




W:-:- .■:■.> ■^.•:-- J 




Fig. 74.— Gonococci contained in Pus Cells. 
From a case of gonorrhceal urethritis. 

abundant during the acute stage of the inflammation. This rather 
large coccus is prone to occur in pairs, and is characterized morpho- 
logically by the flat sides of the individuals as they lie against each 
other (see Fig. 75). They are apt in exudations to be grouped within 
the bodies of cells, but may lie apart. Artificial cultures have been 
made of the gonococcus, which grows only at the temperature of the 
body, and best on human blood serum, on which it forms minute 
thin, grayish, smooth colonies which readily die off. Animals are 
(piite refractory to its inoculation, though suppurative peritonitis 
has been induced in mice and guinea-pigs after intraperitoneal injec- 



166 THE INFECTIOUS DISEASES. 

tion of cultures. Inoculation of cultures on mucous membranes in 
man has been followed by characteristic catarrhal inflammation. 
There is little doubt, from the evidence now at hand, that the go- 
nococcus stands in a causal relationship to the characteristic in- 



Fig. 75.— Micrococcus GoNORRHCEiE (Gonococcus). 

flammatory processes with which it is so constantly associated. But 
in what measure this germ, in what measure the pyogenic bacteria, 
may be responsible for the complicating inflammations when both 
occur together, is not yet known. Tlie gonococcus is readily stained 
by the anilin dyes. 



ANTHRAX. 

Synonyms. — Splenic fever ; Malignant pustule ; Charbon ; Car- 
buncle. 

This disease, which is much more common in the lower animals, 
especially the herbivora, than in man, is of infrequent occurrence in 
the United States, but seems in certain regions to be more common 
than formerly. 

It is induced in man by accidental inoculation with the Bacil- 
lus anthracis, which causes the disease in the lower animals. Inocu- 
lation may occur through the skin by the agency of flies which 




Fig. 76.— Anthrax— Malignant Pustule— of the Skin. 

From a man in New York who had been handlin;^ foreign hides. Bacilli stained with gentian 
violet. 



have been feeding on animals infected with this disease, by handling 
their carcasses or hides, or in other wavs. Followinor this skin inocu- 
lation a pustule is apt to develop— "nialignant pustule " — and vary- 
ing phases of an acute exudative inflammation, Avhieh may be 
hoemorrhagic, sero-fibrinous, purulent, or necrotic, accompany the 
local proliferation of the germs (Fig. 70). From this local source a 
general infection may ensue. In some cases general infection may 
occur without evident external lesion. 

Infection with anthrax mav occur throuii-h the luuu-s, most often 
among those who handle infected wool or hides, the dust from which 



168 



THE IXFECTIOUS DISEASES. 



is inhaled (•'•'wool-sorters' disease"). Under these conditions there 
may be oedema, lobular pneumonia ^rith involvement of the pleura, 
mediastinum, and other adjacent structures. Infection through the 
gastro-intestinal canal occurs through the ingestion of food contain- 
ing anthrax spores, and is apt to be accompanied vrith inflammatory 
and necrotic changes, which are described in detail among lesions of 
the intestine. 

AVhen general infection occurs the post-mortem appearances vary. 

Decomposition, as is usual in a;Cute infections, generally sets in 
early. The blood is frequently not much coagulated and dark in 
color. Haemorrhages and ecchymoses are frequently found in the 









c 



^a?^ 



^^^'' 












Fig. rr.— Bactllits Anthbacis geowixg in the Blood Vessels of the Liver of a Mouse 

EfOCITLATED 'WTTH A PtEE CULTURE OF THE BACILLUS. 



serous and mucous membranes and in various other parts of the 
body. 

The lungs may show small hsemorrhages and oedema, and the 
bronchi may be deeply congested. The pleural cavities may contam 
serum. The intestines may exhibit the lesions of the so-called intes- 
tinal mycosis (see page 47T). The bronchial and other lymph nodes 
mav be swollen. The spleen mav be swoUen. verv dark in color, 
and soft, sometimes almost diffluent. 

The bacillus which causes the disease may be found, usually in 
large numbers, in the spleen and in the capillary blood vessels, 
especially in the hver (see Fig. 77), lungs, kidneys, and intestine. 

The BaciUus anthracis is from five to twenty }.i long and about 
one f.i broad, and is often slio;htlv curved. The ends of the bacilh 



THE INFECTIOUS DISEASES. 100 

are not rounded, but square or slightly concave, and they often hang- 
together end to end, forming thread-like structures (see Fig. 78). 
While the bacilh in the vegetative condition are easily killed, they de- 
velop spores outside of the body which are very invulnerable to the 
action of the ordinary germicidal agents and to heat. They are im- 
mobile and readily stained by the anilin dyes. The anthrax bacillus 
is readily grown on artificial culture media at ordinary room tempera- 
tures, fluidifying gelatin and usually growing out, before it does so, in 
a network of delicate lines into the solid medium. These linear or 
thread-like outgrowths from a central colony give in puncture plants 
in gelatin tubes a brush-like appearance which is quite characteristic. 
Surface colonies on agar and gelatin plates show a delicate, felt-like 




Fig. 78.— Bacillus Anthracis. 

outgrowth from the central mass. The growth on potatoes is volu- 
minous. Inoculations of the anthrax bacillus into various species of 
animals produce the disease. White mice are most susceptible, then 
guinea-pigs and rabbits. In the blood of the diseased animals mul- 
titudes of the bacilli are found, showing their proliferation in the 
blood vessels and elsewhere. They are of especial interest and im- 
portance because we know more of their life history than of almost 
any other of the bacteria, and because it was this bacterium which 
was first absolutely demonstrated to be the cause, and the only cause, 
of a well-defined disease in man. 

The virulence of the germ may be greatly reduced by an exposure 
of cultures for several weeks to a temperature of 42° to 43° C. By 
inoculation with cultures thus artificially treated, animals may be 
rendered immune to infection from virulent anthrax germs. 



TUBERCULOSIS, 

Persons are said to have tuberculosis when there are going on in 
the body inflammatory and necrotic processes accompanjdng and de- 
pendent upon the presence and growth of the tubercle bacillus. 

The difference between this and other forms of inflamjnation in- 
cited by bacteria appears to be largely due to peculiar biological 



.1. f 



^'n< 
















W-y- 




^'3 
W-^-' 






aK^- 



y-r-'^': 



1^ 









^:^> 











i^-'t-.'^ -o, , 





Fig. 73.— a NoDtT,E of Tuberchlab Inflammation O Ttt.tat ;y Txtbercle) in the Lung. 
Showing polyhedral cells, small cells, giant cells, and coagulation necrosis at the centre. 



characters of the tubercle bacillus, and the stimulating and poison- 
ous effects which are produced upon the tissues as the result of its 
metabolism. 

The effect on the body cells of the presence and growth of the 
tubercle bacillus varies considerably, depending upon the number 
and ^arulence of the germs present, the character of the tissue in 



THE INFECTIOUS DISEASES. 171 

which they lodge, and the vulnerabihty of the individual. In gen- 
eral, it may be said that the bacilli stimulate the connective-tissue 
cells in their vicinity to proliferation, and may excite emigration 
of leucocytes from neighboring blood vessels. In this way either 
sharply circumscribed or diffuse growths of new tissue may occur. 

These new tissue growths may consist simply of polyhedral cells, 
or of these together with cells resembling leucocytes, and with either 
or both of these cell forms there may be developed a fibrous stroma. 
Giant cells may be associated with the other cell forms. ^ Blood 
vessels do not, as a rule, develop in the new tissue. There is 



■n - 



.^^r _ ,-, — ,^- ^;, ^~f-7^''Vt':\~-' 






{ '■■'■;' '" .''■■'" ' ■■' ■■'■ ^:^ , , -' ,• "' ■: ^\ -■■ - , I 

I : -. •■■■ .' . - ■ -' ■. ■- '-■■■ ■ '^ ' ^ ■ -:j 

K> , ' , -■'■..■',•■ , . ■ ■ - . - ; 

c .. ,^ _ ■ , ■ ., .■■■■,,,'■ -■".■■• 

i^ ' " '' , ' 

r .^/ • 

^. \ . ' -''' V ■ ■ .. ./ -^. : ■ "^ -a:':v-, 

vt , ''■'',:,, '^ . ' ■ ' '■ '' . • ■ ' "■ 

Fm, 80.— A Miliary Tubercle from a Lymph Node, x 850 and reduced. 
The giant cells are enclosed by the basement substance. 

always a tendenc}" for the occurrence of coagulation necrosis in 
the new-formed tubercle tissue (Fig. 70). This may come on early 
or late, and be moderate or extensive. The tubercle tissue may per- 
sist for a long time in the condition of coagulation necrosis, or it 
may in this condition disintegrate and form larger or smaller cavi- 
ties, ulcers, etc. 

Tuber culosis occurs most commonly in the form of a tubercular 

^ For an account of giant cells, which are found under various conditions and 
are by no means confined to tubercular inflammation, consult 2farchandy Yirchow s 
Archiv, Bd. xciii., p. 518. 



1 1 </ 



THE INFECTIOUS DISEASES. 



inflammation affecting some one part of the body — ^^ localized tuber- 
culosis/"' Such a localized tuberculosis may retain throughout the 
characters of a local inflammation ; it may be accompanied by the 
clinical e^^dences of systemic infection ; it may give rise to the suc- 
cessive development of tubercular inflammation in other parts of the 
body ; it may give rise to a sudden development of tubercular inflam- 
mations in many parts of the body at the same time. 

It seems probable that such localized tubercular inflammations 
are due to the presence of the tubercle bacillus acting as a local irri- 
tant. IS'ot infrequently an already existing simple inflammation be- 



vr"' 








^.m^ 



■'' t^&^ 



^1* 






%■ 



^.../^.<2?f;S=5> 




^ X 



Fig. 81.— Diffuse Tubercle Tissue proji acute Phthisis, x 1,500 and reduced. 



comes tubercular by the secondary lodgment at its seat, and action 
there, of the tubercle bacillus. 

A general infection may be caused by the diffusion through the 
body of bacilli derived from a local tuberculosis, such as tubercular 
phlebitis or arteritis, or from the breaking into a vessel of a tubercu- 
lar lymph node, or by the inhalation into the lungs of large num- 
bers of bacilli. 

The forms of inflammation which are excited by or accompany 
the tubercle bacillus are the exudative and the productive. 

The inflammations run an acute, subacute, or chronic course. 



THE INFECTIOUS DISEASES. 



173 



The lesions which we regularly find are : 

1. Miliar;} tubercles. 

2. Diffuse inflammation of various kinds, with cheesy degenera- 
tion of the inflammatory products. 

3. The ordinary products of inflammation — pus, fibrin, serum, 
epithelium, granulation tissue, and connective tissue. 

Associated with all these lesions we find the tubercle bacilli. 

1. Miliary luhercles. — These are small nodules, of irregularly 
spheroidal shape (Fig. 80), the smallest hardly visible to the naked 
eye, the largest as large as a pea. The smaller ones are gray and 






^i^^^/W^3^^^1i5j;Sfe^^iE^:-v -. 




Fig. 82.— a Tubercle Granulum from the Pleura, x 850 and reduced. 
The giant cells form part of the basement substance. 

semi-transparent ; the larger are opaque, whitish or yellow, especially 
at their centres. 

Miliary tubercles do not all have the same structure. 

Some are composed of granular matter, of degenerated ^-isceral 
tissue, and of epithelial cells and pus. 

Some are composed of a tissue resembling granulation tissue. 

Some are composed of tubercle tissue, alone or associated Avith 
other inflammatory products. 

The term " tubercle tissue '' is employed to designate an inflam- 
matory product which somewhat resembles granulation tissue. It is 
16 



i;-i THE IXFECTIOrS DISEASES. 

composed of a basement substance and of cells (Fig. 81). The base- 
ment substance is delicate and finely granular, and contains round 
and oval nuclei. This basement substance has a reticulated arrange- 
ment, and in the spaces of the reticulum are polyhedral, nucleated 
cells. There may also be present the large nucleated bodies called 
giant cells. These giant cells do not always present exactly the same 
appearance. Some of them seem to form part of, and to be continu- 
ous ^vith, the basement substance (Fig. 8'2) ; others are separated from 
the basement substance, and look hke large cells contained in the 
meshes of the basement substance. In some tubercle tissue the base- 
ment substance, in others the polyhedral cells, iu others the giant 
cells, are predominant. 

Such tubercle tissue is arranged in the form of small spheroidal 
bodies — tubercle granula — and of a diffuse tissue. So that a mihary 
tubercle may be composed of one or more tubercle granula and of 
diffuse tubercle tissue, to "vrhich may be added other inflamma.tory 
products. 

]\Iiharv tubercles mav undero;o cheesv de^'eneration. or. more 
rarelT. be chans-ed into connective tissue. 

The mihary tubercles formed of granular matter or of indifferent 
round-celled tissue are most common in acute general tuberculosis. 
The mihary tubercles formed of well-defined tubercle tissue are most 
completely developed in localized tuberculosis. 

Tubercle tissue infiltrates and replaces connective tissue : it fills 
caA~Lties. and it projects from free surfaces. It contains but very few 
blood vessels, and when it infiltrates a tissue the vessels of that tissue 
become obliterated. There is often associated with it a prohferation 
cif the endothehal cells of the arteries or an obhterating endarteritis. 

If there is a sudden formation of miliary tubercles in many parts 
of the body at the same time, the patient is said to have '* general 
mihary tuberculosis.'' 

2. Diffuse Inflammation icitJi Cheesy Degeneration of the I/i- 
flammatory Products. — This form of lesion is found in the large 
tubercular masses in the brain, in the mucous membrane of the bron- 
chi, in large fiat masses on the serous membranes, and in the diffuse, 
cheesy infiltration of the kidneys, the ureters, bladder, prostate, tes- 
ticle, and uterus. The constant feature of the lesion is the develop- 
ment of an indifferent round-celled tissue which rapidly undergoes 
cheesy degeneration. Embedded in this tissue there may be tubercle 
granula. AVhen the lesion is far advanced the degenerative changes 
may involve all the infiammatory products, so that we find no 
formed elements, nothing but a diffuse, caseous mass. In the earher 
stages of the lesion the indifferent round-celled tissue and the tuber- 
cle granula are readily demonstrated. 



THE INFECTIOUS DISEASES. 175 

3. Pus, fibrin, serum, epithelial cells, connective tissue, and 
indifferent tissue are all found in varying quantities, either separate- 
ly or together, in those parts of the body where tubercular lesions 
have been developed. 

Swelling of the endothelium of blood vessels is frequently occa- 
sioned by the presence in the tissues of the tubercle bacillus. 

The Tubercle Bacilli are slender, filamentous bacteria (Fig. S3), 
varying in length from one-fourth to one- half the diameter of a red 
blood cell. They are frequently curved and bent, and may form 
short chains. They are immobile and stain with difficulty. They 
do not grow at ordinary temperatures, but at the temperature of the 
body on coagulated blood serum or on five-per-cent glycerin-agar or 



N 








Fig. 83. - Tubercle Bacilli, with Pus Cells, in Sputum. 
From a case of tubercular inflammation of the lungs. The bacilli stained with fuchsin. 

on glycerinated beef tea they grow slowly, forming voluminous dry. 
scaly masses or wrinkled pellicles. Usually from two to three 
weeks elapse before any considerable growth occurs on artificial cul- 
ture media. The tubercle bacillus does not grow in nature outside 
the bodies of iTian and certain warm-blooded animals. It may retain 
its vitality for many weeks in the dried condition, but is killed by an 
exposure of fifteen minutes to the temperature of boiling water. The 
tubercle bacillus differs from most similarly formed bacilli in the 
tenacity with which it retains the color when once it has been stained 
with anilin dyes,' and by a special mode of staining its identity is 
commonly established (see below). 



' The bacillus of leprosy has the same property (see page 183). 



176 THE INFECTIOUS DISEASES. 

It is, however, the effect of the h^-ing bacilli upon the organism, 
when introduced into it under favorable conditions, which furnishes 
the only absolute proof of their identity. Inoculation into guinea- 
pigs, rabbits, and other animals of h^-ing cultures of the tubercle 
bacillus is regularly followed by a development of the characteristic 
lesions of the disease. 

It has been f oimd that tubercle bacilh which have been kiUed by 
boiling, when introduced into the body of the rabbit either beneath 
the skin, into the serous cavities, or into the blood vessels and the air 
spaces of the lungs, are capable, as they slowly disintegrate, of stimu- 









- _ -' or :»»' 













Fig. 84. — Jjtplammatory Noditle CPsetdo-Tubercle) rs the Liver of the Rabbit, pboducee 

BY THE LsTRAVEXOUS IS'JECTIOX OF DEAD TuBERCLE BACILLI. 

Most of the dead bacilli have disintegrated, setting free the bacterial proteid pecuhar to this 
germ, -R-hich has stimulated the ne\7 cell growth. A few fragments of the bacilli, however, still 
remain. 

lating the cells of the tissues where they lodge to proliferation, and 
to the j)roduction of new tissue morphologically identical with tu- 
bercle tissue in its various phases (Fig. 84). Coagulation necrosis, 
however, does not occur. Dead tubercle baciUi are also markedly 
chemotactic and capable of causing local suppuration and abscess. 
These effects seem to be due to a peculiar proteid constituent of the 
protoplasm of the tubercle bacillus. 

1 For further details concerning the effects of dead tubercle bacUli in the body see 
Prudden and Hodenpyl, Xew York Medical Journal, June 6th and 20th, 1891, and 
Frudden, ibid., December 5th, 1891. 



THE INFECTIOUS DISEASES. 177 

The number of bacilli which are present in the lesions of tuber- 
culosis is subject to great variations. They are usually abundant in 
the walls and contents of phthisical cavities, and in tubercle tissue 
which is undergoing cheesy degeneration and disintegration. In 
these situations they may be found in myriads, forming sometimes a 
large part of the disintegrated mass. They are found in cells and 
scattered among them. Sometimes they are present in considerable 
numbers in the giant cells of miliary tubercles. In the acute 
general tuberculosis of children they are often present in enormous 
numbers, particularly in the lungs. They may be found in tubercu- 
lar inflammation in any part of the body, and have been seen in 
the blood. The bacilli are almost constantly found in the sputa of 
patients suffering from pulmonary tuberculosis, and their presence 
sometimes affords valuable diagnostic aid in early stages or obscure 
forms of the disease. 

Under a variety of conditions, especially in the older tubercular 
lesions, the bacilli may not be demonstrable. This apparent occa- 
sional absence of the bacilli is probably due either to their disappear- 
ance as the process grows older, or to some unknown changes which 
interfere with the ordinary staining procedures. 

In human beings cases of direct local inoculation of tuberculosis 
have been reported, but they are not very common. 

There seems to be no doubt that the bacilli can be introduced 
into the alimentary canal by infected milk and meat. It is still un- 
certain, however, how often such a mode of infection really takes 
place. 

The ordinary way for tubercle bacilli to be introduced into the 
human body seems to be by the air inspired into the lungs, charged 
with infectious dust. Dust in rooms and places frequented by un- 
cleanly consumptives ma}^ become infectious by an intermingling 
with its particles of floating particles of dried sputum containing 
the living bacilli. 

METHODS OF STAINING THE TUBERCLE BACILLUS. 

In Fluids. — For the examination of fluids, such as sputum, 
etc., the material should be spread in a thin layer on a cover glass, 
dried in the air, and then passed thrice through the flame (see page 

i;io). 

A variety of methods are in vogue for staining the tubercle bacil- 
lus, most of them being more or less unessential modifications of the 
original process formulated by Koch and Rhrlich. The staiuin^- 
fluid which we have found most generally useful is known as Ziohl's 
solution. This is made by adding to a flve-per-cent aqueous solution 



178 THE INFECTIOUS DISEASES. 

of carbolic acid about one-tenth, its volume of saturated alcoholic so- 
lution of fuchsin. This carbolic fuchsin "will keep unchanged for a 
long tirae. 

The prepared cover glass is floated in a watch glass or porcelain 
capsule — specimen side down — on this coloring fluid, and gently 
boiled for from three to five minutes. 

The entire specimen is thus completely stained, tubercle bacilli, 
tissue elements, and other bacteria which may be present, all in the 
same way. The next step is to remove the color wdth acid from all 
the structures which may be intermingled with the tubercle bacilli; 
the latter, owinGf to the tenacitv with which thev retain the color, 
being but slightly affected. This is done by dipping the cover glass 
into an aqueous or alcoholic solution of five-per-cent sulphuric acid, 
and shaking it about for a few seconds. The acid may be even a 
little more dilute than this. Under the influence of the acid the 
specimen on the cover glass loses its red color and becomes gray or 
colorless. It is then thoroughly rinsed in three or four successive 
portions of alcohol, and finally in water. By this manipulation the 
red color may be to a slight extent restored. 

Care should be taken not to expose the specimen too long to the 
action of the acid, because then the bacilli may be also partially or 
completely decolorized. A little experience will enable the experi- 
menter to judge of the proper time for the action of the acid. 

The specimens may be studied in water ^vith the use of a high- 
power lens — preferably an oil immersion — and the Abbe condenser, 
or they may be dried in the air and mounted in balsam. 

Inasmuch as not infrequently some other bacteria besides the 
tubercle bacilli retain a slight red color, it is well, after the specimen 
is rinsed in Tv^ater, to float the cover glass for a few minutes in a 
dilute aqueous solution of methylen blue, which ^vill replace the red 
color in all of the bacteria except the tubercle bacilli, thus forming a 
marked color contrast between them. 

Various other anilin dyes may be used instead of the fuchsin, and 
there are various minor modifications of the process which are often 
employed ; but, on the whole, for routine sputum examinations we 
recommend the method here given. 

In Sections. — Thin sections of tubercular tissue which has been 
hardened in alcohol are stained in the same way, except that instead 
of hastening the process by heating, w^hich is apt to shrivel the sec- 
tions, they must lie in the dye for from twelve to twenty-four hours. 
After decolorization bv acid and dehvdration bv alcohol the sections 
are cleared in ofl of cloves and mounted in balsam. In specimens 
prepared in this way the bacilli stand out as sharply defined slender 
rods or filaments on the uncolored or but slightly tinted background. 



THE INFECTIOUS DISEASES. 171:» 

For purposes of simple recognition of the bacilli in sections it 
seems to the writer usually better to have no color in the preparation 
other than that which the tubercle bacilli possess. But it is often 
convenient to demonstrate the nuclei of the cells at the same time, 
and this may be accomplished by staining lightly afterward with 
a dilute solution of some color which will contrast with that of the 
bacilli, such as Bismarck brown or methylen blue. ' 

^ The anaouncement of the discovery of the Bacillus tuberculosis by Koch was 
made in the Berliner klin. Wochenschrift, 1882, No. 15. A most elaborate and 
valuable article on the same subject by Koch is contained in the " Mittheilungen aus 
dem Kaiserlichen Gesundheitsamte," vol. ii. 

The very voluminous literature on the subject of the tubercle bacillus which has 
accumulated since 1882 is for the most part scattered through the German, English, 
and French journals. It may be best obtained by consulting files of the Index Medi- 
cus of dates since April, 18S2, or Baumgartens " Jahresbericht uber die Forischritte 
in der Lehre von den pathogenen Mikroorganismen." 



LUPUS. 

This form of inflainniation most frequently occurs in the skin of the 
face, but also in the mucous membrane of the mouth, pharjTix, con- 
junctiva, vulva, and vagina.. The lesion consists of small, multiple 
nodules of new-formed tissue, somewhat resembling granulation tis- 




1 -._ ^^r^-,^ jet %xr^ ^ 

«• ^«C« » »^ -a * *»^ 

-^* -^*w* ***** ' *t^i'~' r***--^*^ 










Fig. 85.— Lupus of Face. 

sue, in the cutis or mucosa and submucosa. By the formation of new 
nodules and a more diffuse cellular infiltration of the tissue between 
them, the lesion tends to spread, and by the confluence of the infil- 
trated portions a dense and more or less extensive area of nodular in- 
filtration may be formed. There may be an excessive production and 



THE INFECTIOUS DISEASES. 181 

exfoliation of epidermis over the infiltrated area, or an ulceration of 
the new tissue. 

Microscopical examination shows the lesion to consist in the for- 
mation of tissue composed of small spheroidal cells intermingled 
with variable numbers of larger, so-called epithelioid cells and cell 
masses, and in many cases with giant cells (Fig. 85). In some 
cases a well-marked reticulum is present between the new cells, and 
these are often grouped in masses around the blood vessels. In some 
cases there is, without previous ulceration, a formation of new con- 
nective tissue in the diseased area, and a well-marked cicatrization ; 
in other cases the cells and intercellular substance undergo a disin- 
tegration which leads to ulceration. 

The morphological characters of the lesion long ago led to the 
conjecture that lupus was in reality a form of tubercular inflamma- 
tion. This view has now become established by the numerous obser- 
vations which show the very constant presence of the tubercle ba- 
cillus in small numbers at the seat of inflammation. It is not 
unlikely, however, that in the clinical group of diseases called lupus 
there may be lesions which are not caused by the tubercle bacillus. 
More exact bacterial studies must be made before this point can be 
fully decided. 
17 



LEPROSY. 

Lepra (Leprosy). — This form of mflammation is characterized by 
the development of nodular and sometimes diffuse masses of tissue, 
consisting of larger and smaller cells of various shapes — spheroidal, 
fusiform, and branched, with a fibrous stroma — the whole somewhat 
resembling granulation tissue. The new tissue is most frequently 
formed in the most exposed parts of the skin, as the face, hands, 
and feet, but it may occur in the skin of any part of the body. It 
is formed more rarely in the subcutaneous connective tissue, in in- 
trafascicular connective tissue of nerves, in the ^nscera, and in the 
mucous membranes. The mucous membranes most frequently af- 




FiG. 86.— The Bachjj of Leprosy. 
Stained with gentian violet. From a nodule in the skin. 

fected are those of the eye, nose, mouth, and larynx. The nodules 
may be very small or as large as a walnut, and may be single or 
joined together in gToups or masses. The tissue of the part in which 
the new formation occurs may be atrophied and replaced by, or may 
remain intermingled ^vith, the leprous tissue, or it may be hypertro- 
phied. The nodules may persist for a long time without undergo- 
ing any apparent change, or they may soften and break down, form- 
ing ulcers ; but ulceration, except in the mucous membranes, is said 
usually to occur as the result of injury or unusual exposure. The 
leprous tissue may change ^vithout ulceration into cicatricial tissue, 
or cicatrization may follow ulceration. 



THE INFECTIOUS DISEASES. 183 

Various secondary lesions and disturbances of nerve function are 
associated with the formation of leprous tissue in the nerve and cen- 
tral nervous system, but these we cannot consider here. 

In all the primary lesions of leprosy, bacilli are said to be pre- 
sent, mostly in the cells, and particularly in the larger transparent 
spheroidal forms, but sometimes free in the intercellular substance. 
The bacilli have been found in the skin, mucous membrane of the 
mouth and larynx, in peripheral nerves, in the cornea, in cartilage, 
in the testicles, and in lymph nodes. Sometimes the cells contain 
but few bacilli, but they are frequently crowded with them. The 
bacilli are from 4 to 6 /i long and very slender, being usually less 
than 1 /f in thickness. They are sometimes pointed at the ends and 
sometimes present spheroidal swellings (Fig. 86). They are capa- 
ble of spontaneous movement. In their comportment toward staining 
agents, as well as in general morphological characters, they consid- 
erably resemble the Bacillus tuberculosis, but they are more readily 
stained. They may be stained with f uchsin or gentian violet by the 
ordinary method, or by the method employed for staining the tuber- 
cle bacillus. 

According to ITeisser, the lepra bacillus may be artificially culti- 
vated at body temperature on blood serum and on boiled eggs. 

It is said to grow on glycerin-agar with two per cent of sugar. 
in tubes sealed to retain the moisture. ' 

Animal inoculations have not as yet given positive results. 

The reasonable conjecture that the Bacillus leprae causes the le- 
sions of leprosy depends as yet largely upon the constancy of its 
occurrence in the disease, its absence under other conditions, and 
upon its relations to the cells of the new growth. 

The structure of the new growth, the absence of coagulation ne- 
crosis, and the peculiar grouping of the bacilli in the large transpa- 
rent cells are characters which usually clearly distinguish the lesions 
caused by the leprosy bacillus from those of tuberculosis. 

' Byron, New York Pathological Society, January 27th, 1892. 



SYPHILIS. 

This form of inflainination is in many respects morpliologicall}' 
similar to the tubercular and is probably due to the presence in the 
body of some form of bacteria. That this is so, however, we do not 
certainly know ; we only judge of its probability by inference. The 
characteristic lesion of syphilis consists in a more or less circum- 
scribed formation of new tissue. This new tissue may be made up 
largely of small spheroidal cells, or of these with polyhedral cells 
(Fig. 87), and of occasional giant cells. All of these new cell 




Fig. 87.— Small Nodule of Syphilitic Inflammation (Miliary Gumma) in the Livek. 

masses, which may be very small or occupy large areas, tend to 
undergo coagulation necrosis and to disintegrate at the centres. 
They may be converted into cicatricial tissue. The new tissues in 
syphilitic inflammation contain, as a rule, few blood vessels. It may 
form diffusely or in circumscribed masses. The endothelial cells of 
the blood vessels near the inflammatory foci in syphilitic inflam- 
mation are not infrequently swollen and may proliferate (Fig. 88). 
The vessels may othermse undergo extensive changes. 



THE INFECTIOUS DISEASES. 185 

In the primary lesion, which is called chancre, there is a small 
spheroidal-cell infiltration of the connective tissue, proliferation of 
connective-tissue cells, and an occasional development of ^ant cells. 
This new tissue may become necrotic or ulcerate or become cica- 
tricial. 

Following the primary lesion there may be inflammation of the 
lymph nodes, of the skin and mucous membranes, of the bones and 
viscera. 

One of the most characteristic phases of the secondary inflamma- 
tions of syphilis results in the formation of masses of new tissue 
called gunimata. 

The smaller gummata consist of a mass of small spheroidal 
and epithelioid cells (see Fig. 87). As these cell masses grow larger 







^''^.% t1 










FiG. 88.— New- FORMED Tissue in Syphilitic Inflammation. 
From a " hard chancre," showing swollen endothelium in a small blood vessel. 

they are apt to become necrotic at the centre, and we may then have, 
as seen by the naked eye, a grayish-white, usually firm mass, Avith 
a more or less dense and irregular cheesy centre and a translucent, 
often radially striated border of dense fibrous tissue (see Fig. *24:). 

A bacillus closely resembling the tubercle bacillus in form and 
size has been described by Lustgarten and others as occurring in the 
lesions of syphilis. It is found in very small numbers. A distinctly 
characteristic mode of staining is not known, audit has never been 
cultivated on artificial media ; so tluit the evidence that this bacillus 
is the cause of syphilitic inflammation does not appear to us at all 
convincing. 

For further details regarding syphilitic lesions see Changes in the 
Viscera, Part III. 



RHIXOSCLEROMA. 

This disease, which occurs especially in eastern Europe and 
occasionally in other parts of the world, is a chronic inflammation of 
the nasal, phar^iigeal, and laryngeal mucous membrane. In this 
inflammation a diffuse or nodular formation of new tissue, some- 
what resembhng granulation tissue, occurs, which tends to assume 
a dense cicatricial character. 

Constantly associated with this lesion is a bacillus cahed Bacil- 
lus rhi nosclerom at is. to vrhich the lesion appears to be due. This 
bacillus in many of its morphological and biological characters 
closely resembles the Bacillus pneumoniae of Friedlander. It need 
not be further described here. 



GLANDERS— FARCY. 

These names are given to two varieties of the same disease. The 
disease originates in the horse and occurs in man by contagion. 

In the horse we find four varieties of the disease : chronic and 
acute glanders, chronic and acute farcy. 

1. Chronic Glanders. — The disease begins in the mucous mem- 
brane of the nose. Small, whitish nodules, composed of small 
spheroidal cells, are formed in the mucous membrane. These nodules 
soften and ulcerate. The same nodules may be found in the larynx, 
trachea, and bronchi. The ulcerations may remain superficial, or 
they may extend and attack the subjacent cartilage and bone. Mod- 
ules of the same kind may be found in the lungs. 

2. Acute Glanders. — There is the same formation of nodules, 
which soften and ulcerate ; but they are accompanied with an in- 
tense inflammation of the nasal mucous membrane, and the disease 
runs a rapid course. 

3. Chronic Farcy. — The lymph nodes and vessels become en- 
larged, and nodules are formed in the skin, lungs, and other ^-is- 
cera. The lymph nodes become cheesy, or soften and suppurate. 
The cutaneous nodules soften and suppurate. 

4. Acute Farcy. — There are the same lesions of the lymphatics, 
and nodules and abscesses are found in the skin. There are also nod- 
ules in, and inflammation of, the nasal mucous membrane, and the 
disease runs an acute course. 

In man the disease occurs in an acute and a chronic form, but 
does not exactly resemble any of the varieties of the disease in the 
horse. 

The acute disease runs a rapid and malignant course. The skin 
may be covered with a pustular eruption. Furuncles, carbunclt>8, 
and abscesses are found beneath the skin and in the muscles. Xod- 
ules are found in the nasal mucous membrane, the lungs, kidneys. 
testes, spleen, and liver. The joints may be inflamed, and there may 
be osteomyelitis. 

The disease may begin at a single point, so that it may be mis- 
taken for a, carbuncle or a. gangrenous erysipelas. 

TliL chronic form of the disease is still more ditUcult of diagnosis. 



188 THE INFECTIOUS DISEASES. 

The nodules grow very slowly, are hard, and may occur in groups 
or like a string of beads. The nodules may soften and form chronic 
ulcers. 

A slender bacillus, called Bacillus mallei, has been proven to be 
the cause of glanders both in man and animals. The baciUi occur, 
either scattered or in masses, in the areas of fresh inflammation, are 
less abundant in older foci, and have been found in the blood of af- 
fected individuals. 



^A!'/j 



m 

/•/V- 



Fig. 89. — BAciLLrs ;Maixei. 

The glanders bacillus considerably resembles the tubercle bacillus 
in size and form, but is a httle thicker (Fig. 89). It often occurs in 
pairs or short chains, and is motile. AVhen stained the baciUi often 
show central clear spaces. They grow best at body temperature and 
on the ordinary culture media. The growth is in general somewhat 
viscous. On potato or potato pulp it forms an abundant yellowish 
mass, gradually turning brown. Inoculation of cultures into sus- 
ceptible animals, such as the field mouse, guinea-pig, horse, etc., give 
positive results. The Bacillus mallei, either in culture or in tissue, is 
best stained by Loffler 's methylen blue solution or vnXh. gentian violet. 



TYPHOID FEYEE.^ 

The lesions of typhoid fever are usually well marked and con- 
stant. They may conveniently be divided into two classes : 

I. Those which are characteristic of the disease. To this class 
belong the changes in the lymph nodules (follicles) of the intes- 
tines, in the mesenteric lymph nodes (lymph glands), and in the 
spleen. 

II. Those which are very frequently found vnth this fever and yet 
are not peculiar to it. To this class belong the changes in the parotid 
and pancreas, the degenerations in the liver, kidneys, and voluntary 
muscles, thrombosis of the blood vessels, infarctions, diseases of the 
lungs, and suppuration of the connective tissue in various places. 

I. The Intestines. — The lesions of the intestines consist in an 
inflammatory enlargement and subsequent degeneration of the soli- 
tary lymph nodules and Peyer's patches. 

The process appears to begin with a catarrhal inflammation of the 
mucous membrane, accompanied or immediately followed by changes 
in the lymph nodules. The lesions in the lymph nodules begin early ; 
they have been observed in persons who have died forty-seven hours 
after the commencement of the disease. 

The increase in size of the agminated and solitary nodules may 
be rapid or gradual. The nodules may be onl}" slightly enlarged, or 
may project so as to fill up the cavity of the intestine. The enlarge- 
ment is usually more marked in the agminated than in the solitary 
nodules. Usually the whole of a Peyer's patch will be enlarged, but 
sometimes only a part of it. If the enlargement is gradual the 
different nodules which make up a Peyer's patch are enlarged, while 
the septa between them remain but little changed and give the patch 
an uneven appearance. 

The patches which are only moderately enlarged are of reildish or 
reddish-gray color, are soft and spongy, and their edges blend grailu- 
ally with the adjoining mucous membrane. The patches which are 
more intensely affected ariM^f gray or bnnvnish color, o^ firm consis- 
tence, and rise abruptly fn)m the surrounding mucous nuMubrane, or 



' The most complete doscript ion of the lesions of typhoid fever is that given by 
Ifoffmann, " Abdominal Typhus," 1S(U). 

18 



190 THE INFECTIOUS DISEASES. 

even overhang it like a mushroom. The largest patches are some- 
times more than three-eighths of an inch thick. 

The enlargement and infiltration may spread from the patches to 
the surrounding mucous membrane, so that the patches appear very 
large; a number of them may become fused together, and there may 
be even an annular infiltration entirely around the lower end of the 
ileum. 

The infiltration of the Peyer's patches may also extend outward 
into the muscular coat, and even appear beneath and in the peritoneal 
coat as small, gray, rounded nodules. This condition is usually 
found only with a few patches in the lower end of the ileum ; some- 
times in the caecum and appendix vermiformis. These little gray 
nodules usually correspond to diseased patches beneath them ; some- 
times they appear to excite an inflammation of the peritoneum, 
accompanied by the production of numbers of similar nodules all 
over that membrane. Hoffmann describes a case in which the inflam- 
mation extended to the pleura, with the production of similar nodules 
there. 

The solitary nodules are affected in the same way as Peyer^s 
patches. They may be hardly enlarged at all, or be quite prominent, 
or may be affected over a larger portion of the intestine than are the 
patches. Very rarely the solitary nodules are enlarged, while the 
patches are not at all or but slightly affected. 

The inflammation and enlargement of the agminated and solitary 
nodules are followed by a healing process. The character of this 
process varies according to the intensity of the previous inflammation. 

1. If the disease was mild and the enlargement of the nodules 
moderate, the enlargement gradually disappears and they resume 
their normal appearance. 

2. In moderate enlargements the retrograde processes affect first 
the nodules, and leave the septa between them still swollen and 
prominent. This gives to the surface of a patch a reticulated ap- 
pearance. After a time, however, the entire patch becomes flat- 
tened and uniform. 

3. The solitary nodules or the separate nodules of a patcH soften, 
break down, and their contents are discharged with some attendant 
hgemorrhage. This leaves a bluish-gray pigmentation in the situa- 
tion of each nodule. This pigmentation may remain for years. 

4. In more severe types of the disease the enlargement of the nod- 
ules ends in ulceration. This takes place in two ways : 

(a) The enlarged nodules soften, break down, and discharge into 
the intestine. In this way are formed small ulcers. These ulcers 
increase in size by the same softening process, which gradually at • 
tacks their edges, and in this way ulcers of large size may be formed. 



THE INFECTIOUS DISEASES. 191 

The ulcers may extend outward only to the peritoneal coat, or they 
may involve the peritoneal coat also and perforate, 

(b) In the severest forms of the disease considerable portions of 
the enlarged patches slough, are detached, and leave large ulcers with 
thick, overhanging edges. The slough may involve only the nod- 
ules, or it may involve also the muscular and peritoneal coats. 
These ulcers also may afterward increase in size, and several of 
them may be joined together. 

If the patient recovers the ulcers cicatrize, their edges become 
flattened, their floors a^e converted into connective tissue covered 
with cylindrical epithelium. 

Both forms of ulceration sometimes end in perforation. This is 
effected by the extension of the ulcerative process through the peri- 
toneal coat or by the rupture of the floor of the ulcer. Peritonitis 
and death are the usual result. In rare cases, however, the patient 
recovers and the perforation is closed by adhesions. 

The minute changes which take place in the course of the intes- 
tinal lesion are as follows: 

At first the blood vessels around the nodules are dilated and con- 
gested, while the nodules are swollen and the epithelium falls off. 
Then the nodules increase in size, largely from a growth of new cells. 
The new cells are, in part, similar to the lymphoid cells which nor- 
mally compose the nodules ; in part are large, rounded cells, some 
of which contain several nuclei. The production of new cells is not 
confined to the nodules, but extends also to the adjacent mucous 
membrane. In many cases also little foci of the same cells are 
found in the muscular, subserous, and serous coats. This increased 
number of cells compresses the blood vessels and the parts become 
anaemic. Soon the cells degenerate, either by granular degeneration 
of individual cells or by gangrene of part of a nodule. In either 
case the degenerated portion is eliminated into the intestine and 
leaves an ulcer of which the floor and edges are infiltrated with 
cells. After this the cell growth goes on and the ulcer enlarges, or 
the cells are gradually replaced by connective tissue and cicatriza- 
tion follows. 

The lesions we have described are found most frequently and 
most developed in the lower part of the ileum. Tiiev are not al- 
waj^s, however, confined to this situation. Enlarged and ulooratod 
nodules may be found over the entire length of the ileum and even in 
the jejunum. They may also extend downward and be fouml in the 
colon, even as far down as the rectum. Tlie same changes may also 
take place in the appendix vermiformis. 

Besides the regular typhoid lesions of the intestines wliioh havt^ 



192 THE INFECTIOUS DISEASES. 

been described, we occasionally meet with others of a more acciden- 
tal character. 

Gangrene of the intestinal wall sometimes occurs. It most fre- 
quently involv^es a portion of the wall corresponding to an ulcer, but 
may also affect other portions where no ulcer exists. The process 
may terminate in perforation or in healing. 

Croupous Inflammation may attack the mucous membrane of 
either the large or small intestine. The mucous membrane between 
the typhoid ulcers is covered and infiltrated with an exudation of 
fibrin and pus. 

Peritonitis of a mild type is a frequent accompaniment of the 
intestinal lesions. It appears to have but little influence on the 
course of the disease. 

Severe peritonitis is usually due to perforation, less frequently to 
ulcers which reach the serous coat but do not perforate. Where 
there is infiltration of the serous coat with the typhoid new growth, 
the peritonitis may be accompanied by a production of little gray 
nodules of the same character throughout the peritoneum. 

Infarctions of the spleen, inflammation of the ovaries, and per- 
foration of the gall bladder are sometimes the cause of peritonitis. 

Hcemorrhage from the intestines is merely due to the inflamma- 
tory swelling and congestion of the mucous membrane, and is slight ; 
or it is due to the ulceration of the follicles and destruction of the 
blood vessels, and is then often profuse. 

Mesenteric Lymph Nodes. — The mesenteric nodes undergo the 
same changes as the nodules of the intestines, and are usually affect- 
ed in a degree corresponding to the intensity of the intestinal lesion. 

The nodes are at first congested and succulent ; then there is a 
production of lymphoid cells and large cells (Fig. 223), as in the 
intestinal nodules, and the node becomes enlarged. When the en- 
largement has reached its full size the congestion diminishes and the 
cells begin to degenerate. The degeneration may take place slowly, 
and then the node gradually returns to its normal condition ; or more 
rapidly, and then little foci of softened, purulent matter are formed. 
If the patient recovers the small foci are absorbed, leaving a fibrous 
cicatrix ; the larger foci become dry, cheesy, and enclosed in a fibrous 
capsule. The inflammation of the nodes may produce a local or 
general peritonitis. 

The Spleen. — In nearly every case of typhoid fever the spleen is 
enlarged. This enlargement begins soon after the commencement 
of the disease, increases rapidly until the third week, remains station- 
ary for a few days, and then diminishes. The organ is congested, 
of dark-red color, and of firm consistence while it is increasing in size. 
After it has reached its maximum size its consistence becomes soft 



THE INFECTIOUS DISEASES. I'.r4 

and there is a considerable deposit of brown pigment. The enlarge- 
ment appears to be due to the congestion and to an increase of the 
normal elements of the spleen (compare page 622). 

In rare cases the softened spleen is ruptured, with an extravasa- 
tion of blood into the peritoneal cavity. 

There may be infarctions of the spleen, which sometimes soften 
and cause peritonitis. 

11. The second class of lesions coinprises those which are fre- 
quently found with typhoid fever, but are not peculiar to it. 

The Mouth. — A number of changes are found about this region. 
The follicles at the root of the tongue and the tonsils may be en- 
larged ; the muscles of the tongue may undergo waxy and granular 
degeneration ; gangrenous ulcers may attack the floor and sides of 
the mouth and destroy large areas of tissue. 

The Pharynx may be the seat of catarrhal or croupous inflamma- 
tion, producing saperficial and deep ulcers. 

The Parotid is, in a moderate number of cases, the seat of an in- 
flammation which tends to suppuration. In this process both the 
glandular acini and the connective tissue between them are involved. 
Which of the two has the larger share in the process is still in dis- 
pute. 

A slight enlargement and induration of the parotid and sub- 
maxillary glands is said by Hoffmann to be a frequent lesion, and to 
depend on increase of the gland cells and dilatation of the acini with 
their secretion. 

The Pancreas undergoes changes similar to those in the salivary 
glands. It becomes at first swollen and red, then hard and gra^-ish. 
then yellow. The vessels are at first congested, afterward there is 
increase of the gland cells, and lastly degeneration. 

The Liver may preserve its normal character or may present 
changes. 

In many cases the organ will be found soft and flabby. ]\Iinute 
examination then shows that the liver cells have undergone degene- 
ration. They are filled with fine granules and small fat globules, and 
the degeneration may go on so far that the outlines of the hepatic 
cells are lost and nothing but a mass of granules can be seen. 

Less frequently we find in the liver very small, soft, grayish mxl- 
ules resembling those found in the peritt)neum. They are situated 
along the course of the small veins, and there is at the same time a 
diffuse infiltration of lym})hoid cells along the small veins. The nod- 
ules consist of lymphoid cells ; they are often too small to be distin- 
guished with the naked eye. 

TJie Heart. — In a considerable niunber of cases the muscular tis- 
sue of the heart is altered. The heart ft^els soft and flabbv : it is of 



194 THE INFECTIOUS DISEASES. 

graj^sh or brownish color ; the muscular fibres are infiltrated with 
fine granules, and sometimes with brown pigment. Or the heart is 
firm, but friable and easily torn, its cut surface ghstens, and its mus- 
cular fibres are in the condition of hvalhi deo^eneration. 

Thrombi in the cavities of the heart and vegetations on the valves 
are sometimes found. Detached fragments of these may be lodged 
as emboli in the different arteries. 

The Arteries.^ — There may be an acute inflammation of the ar 
teries, especially at the commencement of convalescence. There are 
two varieties : an obhterating and a parietal arteritis. In the obht- 
erating arteritis there is infiltration of all the coats of the artery, 
^Wth roughening of the intima and the formation of a thrombus 
^^-ithin the vessel, and this is followed by dry gangrene of the parts 
supphed by the artery. In the parietal variety the wall of the artery 
is infiltrated ^vith cells, but the inthxia is not roughened and no 
thrombus is formed. 

The Veins. — Thrombosis of the larger veins, especially of the fem- 
oral vein in the third and fourth weeks of the disease, is not un- 
common. 

The Larynx is very frequently the seat of catarrhal inflamma- 
tion, T^'ith or without superficial erosions. Less frequently there is 
croupous inflammation, followed in some cases by destructive idcera- 
tion. 

The Lungs. — Catarrhal inflammation of the large bronchi is very 
common. Broncho-pneumonia occurs in t^vo forms. There may be 
a severe inflammation of most of the bronchi of both lungs, with cel- 
lular i nfi ltration of the walls of the bronchi and zones of peribron- 
chitic pneumonia ; or there is an intense general bronchitis, with lob- 
ules of the lung corresponding to obstructed bronchi, either cohapsed 
or inflamed, or both. 

From the long-continued recumbent position of the patients the 
posterior portions of the lungs become congested, dense, and un- 
aerated. Sometimes, in addition to this, irregular j^ortions of the 
lungs become hepatized. 

Less frequently there is regiflar acute lobar pneumonia. 

There may be infarctions in the lungs. 

GangTene of the lungs is occasionally found, either associated ^tii 
lobular pneumonia or with infarctions, or as an independent condi- 
tion. 

The Kidneys very frequently present the lesions of acute degene- 
ration. Thev mav contain infarctions. 

^ Bane, Rev. de Med., January, February, 1881. Keen, " Toner Lectures on the 
Surgical Complications of the Continued Fevers," 1877. 



THE INFECTIOUS DISEASES. I9o 

The Ovaries. — Hsemorrhage and gangrenous inflammation have 
been observed in rare cases. 

The Testicles. — Orchitis has been described by OlHvier. ' It 
generally is developed during convalescence ; it is unilateral ; it 
usually affects the testicle alone, less frequently the epididymis ; it 
terminates in suppuration in nearly one -fourth of the cases. 

The Brain. — Acute meningitis, thrombosis of the venous sinuses, 
and obliterating endarteritis of the cerebral arteries are occasionally 
observed. 

The Voluntary Muscles, especially the abdominal muscles, the 
adductors of the thigh, the pectoral muscles, the muscles of the dia- 
phragm and of the tongue, frequently undergo the hyalin degene- 
rative changes described under muscle lesions. 

Tlie Skin. — Gangrenous inflammation of the skin frequently oc- 
curs in the form of bed sores, affecting especially the skin over the 




Fig. 90.— Cluster of Typhoid Bacilli in the Spleen. 

sacrum and trochanters, where it is subjected to the constant pres- 
sure of the bed. 

There may be suppurative inflammation of the connective tissue 
in any part of the body. Perhaps the most important of these local 
suppurations is that which produces retropliar3^ngeal abscesses. 

THE BACILLUS OF TYPHOID FEVER. 

The presence of a bacillus in various parts of the body in typlioid 

fever, in a considerable proportion of the cases examined, has boon 

well established by a largo number of observers. This bacilhis does 

not occur in the body, so far as is known, except in connection with 

this disease. 

In the early stages of the disease the bacillus may be found in the 



> Kev. de Med., Novombir ;uul December, 1883. 



196 THE INFECTIOUS DISEASES. 

lymphatic structures of the intestines and in the mesenteric lymph 
nodes and the spleen. It may be present in the kidney, liver, lungs, 
and in the blood, and is often found in enormous numbers in the in- 
testinal contents. In the viscera it is apt to occur in larger and 
smaller masses or clusters (see Fig. 90). It has been repeatedly 
found in the urine. 

The typhoid bacillus is usualh^ about three times as long as 
broad, being about one-third as long as the diameter of a red blood 
cell. It is rounded at the ends, and frequently contains rounded 
structures which have been regarded as spores, but which further 
researches have led us to believe are not spores but vacuoles. 

The typhoid bacillus can be readily cultivated on the ordinary 
culture media at room temperature. It forms delicate, bluish- white, 
sinuous-edged, spreading colonies on the surface of nutrient gelatin, 
which it does not fluidify. Several other bacteria grow in a similar 
way on gelatin, but the mode of gro^vth of the typhoid bacillus on 
boiled potatoes, as a nearly invisible pellicle, is its most marked cul- 
ture characteristic.^ If, however, the potato be made slightly alka- 



Fig. 91. — BAcrLLUs typhosus. 
From gelatin culture. 

line the surface growth becomes e^adent. In cultures the typhoid 
bacilh often cling together end to end, forming long, thread-like 
structures (Fig. 91). The bacilli in fluids are actively mobile. 

Inoculations of the typhoid bacillus into animals, ^vhile not pro- 
ducing a disease in all respects like that in the human subject, may 
cause death with symptoms and lesions as closely resembling those 
in man as we are often able to produce in animal experimentation. 
Although similar effects may be induced in animals by the inocula- 
tion Avith other germs, altogether the evidence that typhoid fever 
in man is produced by the tyj^hoid bacillus, and by this alone, is so 
strong as practically to amount to a demonstration. 

It is probable that the usual s^miptoms and lesions of. typhoid 
fever are largely due to the absorption of toxic substances which are 
produced as the result of the Ufe processes of the bacteria at the 

' Several bacilli are known which considerably resemble the typhoid bacillus iu 
their form and general biological characters under cultivation. Most noteworthy 
among these is the Bacillus coli communis, which is a constant resident of the gas- 
tro intestinal canal (see page 205). 



THE INFECTIOUS DISEASES. 107 

point of their greatest accumulation and activity, namely, in the in- 
testinal canal. 

Some of the inflammatory complications which occur in tyx)hoid 
fever are due to the growth of the bacillus in unusual places in the 
body/ but many of them are due to a secondary infection with 
other germs, notably with the pyogenic cocci. Infection with the 
typhoid bacillus seems to occur largely through the gastro-intesti- 
nal canal. In a large proportion of cases it is communicated by 
means of food or drinking water which has been polluted with the 
excretions of persons suffering from the disease. 

The bacilli are capable of living for considerable periods in water 
as well as in ice. They have been repeatedly found by biological 
examinations in polluted drinking water to which external evidence 
has pointed as the source of a typhoid epidemic. 

METHODS OF STAINING THE TYPHOID BACILLUS. 

The bacilli, when taken from cultures, stain readily with the or- 
dinary anilin dyes, such as fuchsin and gentian violet (see page 130). 

In sections of the organs they do not take the stain so readily. 
They are decolorized by Gramas method. 

One of the most satisfactory solutions for this purpose is that of 
Ziehl, which is made as follows : 

Filtered saturated aqueous solution of Carbolic Acid, 90 
Saturated alcoholic solution of Fuchsin 10 

The sections are soaked for half an hour in this solution and then 
decolorized by alcohol, cleared in oil of cedar, and moiuited in bal- 
sam. The decolorization should be done carefully, the section being- 
examined from time to time as it proceeds, so as to avoid the removal 
of too much color. The nuclei should remain faintly colored, but not 
so much so as to conceal the clusters of more deeply stained bacilli. 

' Consult Faschiag, Wiener klin. Wocheuscbrift, May otli, 1892. 
19 



DIPHTHERIA. 

Diphtheria is an acute infectious disease caused by the Bacillus 
diphtherice (Loffler), and usually characterized by a pseudo-mem- 
branous inflammation on some of the mucous membranes or occa- 
sionally on the surface of wounds. 

The mucous membranes which are the most frequently affected 
in diphtheria are those of the tonsils, pharynx, soft palate, nares. 
larynx, and trachea ; less frequently those of the mouth, gums, oeso- 
phagus, and stomach. 

The local inflammation may present various pnases, which repre- 
sent clinical types of the disease. Thus there may be a simple red- 
ness of the affected surfaces which leaves no trace after death, or a 

mm 

Fig. 92.— Bacillus Diphtherle. 
yrom a cultiire on agar. 

catarrhal inflammation. On the other hand, in the more marked 
forms of the lesion there may be a fibrinous exudate which infiltrates 
the mucous membrane, or, intermingled with pus cells, epithelial 
cells, red blood cells, bacteria, and granular material, forms a thick 
or thin pellicle on the affected surfaces. This pellicle may undergo 
coagulation necrosis, and hand-in-hand with, this there may be su- 
perficial or deep coagulation necrosis of the mucous membrane. 

The false membrane in diphtheria is thus formed by a combina- 
tion of inflammation and necrosis, the extent of the necrosis and the 
amount of inflammatory products varj^ng in the different cases. 

The pseudo-membrane may disintegrate or exfoliate, with or with- 
out loss of tissue in the underlying mucous membrane. Phlegmon, 
abscess, and oedema are liable to occur as local complications. 
Adjacent and distant lymph nodes are apt to be swollen, and often 
show, on microscopical examination, small foci of cell necrosis and 
disintegration. Similar necrotic foci and areas of small spheroidal- 



THK IXFECTIOL'S DISEASES. 100 

cell accumulation with fatty degeneration may be found in the kid- 
ney and liver. 

Catarrhal bronchitis and broncho-pneumonia or lobular pneumonia 
frequently complicate diphtheritic lesions of the upper air passages 
and fauces. 

Bacteria of various forms are commonly present in the false 
membrane, and some of the forms may penetrate deeply into the 
underlying tissue. The germ, however, which stands in a causa- 
tive relationship to this disease, and which is frequent in the pseudo- 
membrane, is the Bacillus diphtheriiB of Loffler. 

The Bacillus diphtheri?e, first described and definitely associated 
with this disease by Loffler, is from 2. 5 to 3 fx in length and 0. 5 to 
0. 8 ^ in thickness, and is characterized morphologically by marked 
irregularities in its form (Fig. 92). While the typical form is that 




WMm'imi:^^!^m:mm. 













Fig. 93.— Diphtheritic Inflammation of the Tonsil. 
Showing Loffler's bacilli in the pseudo-membrane. 

of a moderately stout, round-ended bacillus, it is very apt — perhaps 
as a result of degeneration — to appear club-shaped, irregularly seg- 
mented, and to develop at the ends a strongly refractile material 
which stains more deeply than the rest of the protoplasm. 

The diphtheria bacillus is innnobile, grows slowly and scantily at 
room temperature, but at body temperature develops rapidly in bouil- 
lon and on agar, glycerin-agar, and blood serum. On glycorin-agar 
plates it grows in the form of moderately small, grayish-white, slight- 
ly spreading, rough-edged colonies. According to Welch aiul A bbott. 
it grows abundantly in an invisible pellicle on potatoes. It doi^s not 
form spores. AVelch and Abbott have found that in fluids it may 
be killed by an exposure of ten minutes to a temperature of oS^ C. 
But it may remain alive for weeks, or even months, in fragments of 
dried membrane. 



200 THE INFECTIOUS DISEASES. 

In man the bacilli are confined to the seat of local lesion, and 
sometimes occur in enormous numbers, especially in the older layers 
of the pseudo-membrane. The systemic effects in diphtheria appear 
to be due to the absorj^tion into the body of a poison elaborated by 
the germs, and presumably a toxalbumin. 

Inoculations of cultures subcutaneously in guinea-pigs are regu- 
larly followed by a localized hsemorrhagic oedema with a variable 
amount of a whitish exudate. Death usually follows the inocula- 
tion in from two to five days. In addition to the local lesions there 
may be — but this is not constant — swelling of the adjacent and of 
the abdominal lymph nodes, serous effusions into the pericardial, 
pleural, and peritoneal sacs, swollen spleen, and acute parenchyma- 
tous and fatty degeneration in the liver, kidney, and heart muscles ; 
congestion and sometimes haemorrhage of the suprarenals. Micro- 
scopical examination shows, in a considerable proportion of cases, 
fragmentation of nuclei and other evidences of cell death at the seat 
of inoculation and in the viscera/ Animals which survive the in- 
oculations may develop later paralysis, and a similar result may fol- 
low the injection into rabbits of culture fluids. The bacilli do not 
gain access to the body at large, but may be found at the seat of 
inoculations. Inoculation into the mucous membranes of rabbits, 
pigeons, and certain other animals may result in the development of 
a pseudo-membrane somewhat resembling that of the disease in man." 

The very frequent association of the pyogenic cocci with the 
diphtheria bacillus gives rise to a complicating series of results which 
make the clinical picture and the lesions of diphtheria sometimes 
very complex. Thus the complicating bronchitis and broncho-pneu- 
monia, as well as pysemic symptoms and lesions, may be due to the 
presence in the pseudo-meixibrane, and the entrance into the deeper 
air passages and the blood, of the Streptococcus pyogenes and the 
Staphylococcus pyogenes. ^ 

The diphtheria bacillus may be stained with Lofiier's alkalin- 
methylen-blue solution or by Gram's method. 

^ For a detailed description of minute cell changes in animals following inocula- 
tion with diphtheria bacilli, see Welch and Flexner, " Histological Changes in Experi 
mental Diphtheria," Bulletin of the Johns Hopkins Hospital, August, 1891. 

- It is important from the prophylactic standpoint to remember that the Bacillus 
diphtheriae may remain alive in the mouth of the human subject for many days after 
recovery from the local lesions of the disease. 

^ Several observers have found, both in diphtheria and under other conditions, a 
form of bacillus almost identical in its general morphological and biological charac- 
ters with Loffler's bacillus, but not virulent on animal inoculation. This is called the 
pseudo-dipMlieritic bacillus, and its exact significance is not very well understood (see 
Abbott," Further Studies upon the Relation of the Pseudo-diphtheritic Bacillus to the 
Diphtheritic Bacillus," Johns Hopkins Hospital Bulletin, October-November, 1891). 



TETANUS. 

This disease is caused by a bacillus which is rather widespread 
and in some places very abundant, occurring with other germs in the 
soil and gaining entrance to the body through wounds, in the exu- 
date from which it may be found. The Bacillus tetani is a rather 
long, slender, mobile germ, prone to develop a spore in one end (Fig. 
94), under which condition the bacillus swells at the end and becomes 
club or racket-shaped. It is readily stained. At the room tempera- 
ture it grows on artificial culture media, and is strictly anaerobic, 




Fig. 94.— Bacillus Tetani. 
From a culture. 

flourishing in an atmosphere of hydrogen. It fluidifies gelatin after 
sending out into it irregular-shaped, ray-like outgrowths. 

Characteristic tetanic symptoms may be induced in mice, guinea- 
pigs, and rabbits by subcutaneous inoculation of cultures. There are 
no characteristic anatomical lesions in tetanus. The bacillus pro- 
duces its effects in the body, both in men and animals, by the elabo- 
ration of a substance which appears to be a toxalbumin. The 
action of this toxic substance appears sometimes to continue in the 
body after the death of the organisms which have elaborated it. 



IXFLUENZA. 
{Epidemic Catarrhal Fever j Grippe.) 

This is an epidemic infectious disease characterized by fever, phy- 
sical and mental prostration, pains in different parts of the body, 
and inflammations of the mucous membrane, lungs, pleura, and peri- 
pheral nerves. 

Influenza has no one characteristic local lesion. There may be 
conjunctivitis, otitis, naso-pharyngeal catarrh, tonsillitis, laryngitis, 
bronchitis, pneumonitis, pleuritis, gastritis, enteritis, or peripheral neu- 
ritis. None of these inflammatory processes appear to have any 
characteristic morphological features. 

The numerous bacterial studies which up to 1892 had been made 
on epidemic influenza had failed to reveal any micro-organism which 
could fairly be regarded as of etiological significance, although some 
of the complicating inflammations, especially of the lungs, had been 
shown to be very frequently associated with the pyogenic cocci — Sta- 
phylococcus pyogenes and Streptococcus pyogenes and the Diplococ- 
cus pneumonise. ^ 

Early in 1892 Pfeiffer, Kitasato, and Canon^ described the occur- 
rence in the bronchial exudate and in the blood of influenza patients 
of a very small bacillus, hitherto unknown or possibly noted earlier by 
Babes. This bacillus was sometimes present in the bronchial exudate 
in enormous numbers, and often with little contamination with other 
germs. In the blood it was sometimes abundant, sometimes scanty. 
It stains with some difficulty with the simple anilin dyes : but 
by Ziehrs solution (page 197) ; or by warmed Loffler's methyl blue 
(page 133); or by Czenzynski^'s fluid (page 68), heated with the sj^eci- 
men at body temperature for from three to six hours, it is readily 
colored. The bacilli are very slender and short (one to one and a 
half times as long as broad), sometimes lie singly, sometimes in pairs 
or short chains or heaps. 

This so-called influenza bacillus grows best at body temperature. 
On glycerin-agar it forms A^ery small, scarcely visible dewdrop- 

^ Consult Finkler, "Die acuten Lungenentziindungen," 1891, p. 452. 

- Deutsclie medicinische Woclienschrif t, January 14tli and May 26th, 1892. 



THE INFECTIOUS DISEASES. 203 

like colonies ; these, although growing close together, do not tend to 
coalesce, as many germs do. It does not grow at a temperature at 
which nutrient gelatin remains solid. In beef tea it forms a scanty, 
€loudy growth. It has been cultivated through several generations, 
but is prone to die off. 

Animal inoculations have given diverse and not very marked re- 
sults. 

These observations have been in general confirmed by Cornil and 
Chantemesse, Babes, Pfuhl, and others.' 

On the whole, we can only say at present that while the occurrence 
of the above-described bacillus in influenza is interesting and appa- 
rently significant, we cannot yet definitely regard it as of established 
importance in the etiology of the disease. 

'^ Cornil and Chantemesse, La Semaine medicale, February 10th, 1892, p. 46. 
Babes, Deutsche medicinische Wochenschrift, February 11th, 1892. PfvM, Central- 
blatt fur Bakteriologie, etc., March 25th, 1892. 



BACILLI WHICH ARE OCCASION"AL I]^CITERS OF 

i:>NrFECTious disease I^ ^LA^. 

Bacillus oedematis inaligni. — This bacillus, which is frequent- 
ly present in dust, in putrefying substances, and in garden earth, 
considerably resembles the anthrax bacillus in form, but is more 
slender and has rounded ends. When it develops spores the bacillus 
is swollen or bellied at the middle. It is strictly anaerobic, growing 
readily in gelatin-agar and blood serum. It fluidifies gelatin. Gas 
is developed in its growth on blood serum. 

Several times this bacillus has been found in persons who have 
received dirty wounds, and it has been associated with hsemorrhagic 
oedema, gas formation in the tissue, and gangrene. Similar lesions 
are produced by inoculation of the pure cultures in animals. 

This bacillus is readily stained by any of the common anilin dyes. 

Bacillus pneumonice (Friedlcuider). — In a small proportion of 
cases of lobar and lobular pneumonia, and in a few cases of exudative 
inflammation of the pleura, pericardiuixi, meninges, and middle ear, 
this bacillus has been found. It is sometimes found alone, but in pneu- 
monia is frequently associated either with the Diplococcus pneumoniae 
or with the pyogenic cocci. It has been found in the nasal secretion 
and mouth of healthy persons. While belonging definitely among 
the bacilli, it so frequently occurs in the form of very short rods or 
ovals or short chains that it was formerly thought to belong among 
the cocci. The bacilli, whether longer or shorter, single or in short 
chains, in cultures as well as in exudates, are surrounded by a nar- 
row hyalin capsule. 

It grows readily, at ordinary room temperature, in gelatin, which 
it does not fluidify, forming a white mass, which, heaping itself upon 
the surface and less markedly along the puncture line, forms a rather 
characteristic ^' nail-like^' growth. It grows abundantly on other 
culture media. It is moderately pathogenic for mice. It seems 
highly probable rather than proven that it may be at least partially 
responsible for the lesions with which it is infrequently associated in 
man. This germ was formerly believed to be of great importance in 
connection with acute lobar pneumonia, and for a time was generally 
spoken of as the pneumococcus of Friedlander. It is now known not 



THE INFEGTIOUS DISEASES. ^Ofj 

to be a coccus, and is certainly of subordinate if at all of serious im- 
portance in the induction of inflammation of the lungs. 

Bacillus coll communis ('' colon bacillus"). — This germ, whic?i 
is of constant occurrence in the intestinal canal of man, is com- 
monly reckoned among the saprophytes. 

It is both morphologically and biologically very similar to the 
typhoid bacillus, to which it appears to be closely related. It is dis- 
tinguishable by several well-marked biological features, as well as 
by its pathogenic power, from the typhoid germ. The points in- 
volved in the differential diagnosis of the colon from the tyj)hoid 
bacillus are too intricate and numerous to be considered here. ' 

Recent studies, especially those of Welch, have shown that not 
infrequently when the Bacillus coli communis finds access to the 
peritoneal cavity or other parts of the body where it does not belong, 
it is capable of inciting serious and even fatal disease. 

In the kidney, in the gall passages, in hsemorrhagic pancreatitis, 
in appendicitis, and repeatedly in peritonitis, as well as in other 
lesions, it has been found either alone or in association with other 
germs. 

It would appear from the observations of Welch, ^ who found it in 
one or more of the organs of the body in thirty-three out of about two 
hundred autopsies, that lesions of the mucous membrane of the in- 
testine, haemorrhage, ulceration, perforation, catarrhal and diphthe- 
ritic inflammation, strangulation, injury, etc., may open the way for 
its access to various parts of the body. In some cases its presence was 
associated with lesions, in some not. On the whole, it would seem 
that we are justifled in regarding the colon bacillus as of occa- 
sional pathogenic importance in man. The limitations of its signifi- 
cance must be determined by further studies. 

^ For literature of differences and similarity between the tj-plioid and colon 
\i2iQ,\\\\ conswM Frambusti, Centralblatt fiir allg. Path, und path. Anat., Bd. iii., Xo. 
8, 1892. Rodct and Eoicx, Arch, de med. Exp., May 1st, 1892. 

^ Welch, "The Bacillus coli communis: The Conditions of its Invasion of the 
Human Body, and its Pathogenic Properties," Medical News, December 12th, 1S91. 
20 



ACTINOMYCOSIS. 

This disease is due to the growth in the body of a micro-organism 
whose botanical position is not quite clear, but which seems to belong 
among the bacteria. This micro-organism, the actinomyces, appears 
to belong to one of the more complex groups of bacteria called the 
Cladotricacese, which develop in the form of branching filaments. 
These filaments in actinomyces frequently separate into longer and 
shorter rod-like or almost spheroidal segments. 

It may be grown on artificial culture media, flourishing best 
at body temperature. It at first develops in the form of delicate. 




Fig. 95.— Actinomyces Bovis. 
Showing one of the yellowish masses of the parasite separated from the surrounding tissue. 



branching threads, the older cultures showing segments which 
resemble bacilli and cocci, and various bulbous, flask-like or club- 
shaped forms which appear to be the result of degeneration ( ' ' invo- 
lution''^ forms) (Fig. 95). Successful inoculations of cultures have 
been made in animals. This micro-organism grows in radiate masses, 
especially in the jaws of cattle, but is of occasional occurrence in man. 
The fungous mass may form a large tumor in the jaw. by its own 
growth and by the formation of granulation tissue, which is apt to 
slough and spread, so that not only may the tissues of the tongue, 
pharynx, larynx, etc. , be involved, but nodules of similar character 
may form in the gastro-intestinal canal, lungs, skin, etc. In man 
suppuration with necrosis and the formation of abscesses, ulcers, and 



THE INFECTIOUS DISEASES. 



207 



fistulse may be the marked accompaniments of its growth in jjarts 
near the surface of the body. 

In the lungs the lesions may be essentially those of an acute gene- 
ral bronchitis or in the form of broncho-pneumonia (Fig. 96), with 
the formation of new tissue. Abscesses and cavities may form 
which extend into adjacent parts. The characteristic masses of the 
micro-organism may be found in the sputum in these cases of acti- 
nomycosis of the lungs. ^ 

In intestinal actinomycosis nodular masses of new tissue with 




Fig. 96.— Actinomyces growing in Human Bronchus. 
The bronchus is filled with a purulent exudate and its wall is becoming involved. 

ulceration may develop in the mucosa and submucosa. ^letastases 
have been described. 

The fungus forms little yellow masses as large as a millet seed or 
smaller, which are scattered through the new-formed granulation 
tissue or mingled with the pus, giving the growths a very character- 
istic appearance. It is the peculiar radiate grouping oi the tilainents 
of the growth (Fig. OG) which gave rise to the Uiune ** ray fungus." 

' For a detailed description of the lung losicnis in ni'tiniMnyeosis, with jreuenil 
bihliogrni^hy, see lUnhnpijI, " ActintMuyeosi.'^ of the I.iin>:." New York Medical 
Kecord, December VM\\, 1800. 



308 THE INFECTIOUS DISEASES. 

The disease is propagated from one animal to another by inoculation 
or by contact of the growth with a wound or an abrasion of the mu- 
cous membrane. The fungous masses may become calcareous. 

In the examination of sputum, faeces, pus, etc., for the presence 
of actinomyces, the naked-eye appearances may be of value, since 
the yellowish-white granules are often quite visible, especially on a 
black background. Suspicious masses may be teased and studied 
unstained, or stained by Gram's method. Sections of tissue contain- 
ing actinomyces may be hardened in alcohol, and sections stained 
by Gram's method with contrast eosin stain. 



ASIATIC CHOLERA. 

In some cases of cholera there are no marked changes to be found 
after death. 

If death occurs during the invasion of the disease or in the stage 
of collapse, in the more marked cases the appearances are as follows : 

The bodies remain warm for some time, and the temperature may 
rise for a short time after death. The rigor mortis begins early and 
lasts for an unusually long time. The muscles sometimes exhibit a 
peculiar spasmodic twitching before the rigor mortis sets in, espe- 
cially the muscles of the hand and arm. 

The Skin is of a dusky gray color, the lips, eyelids, fingers, and 
toes of a livid purple. The ends of the fingers are shrivelled, the 
cheeks and eyes are fallen in. 

The Brain. — The sinuses of the dura mater are filled with dark, 
thick blood. The pia mater may be normal, or oedematous, or ecchy- 
mosed, or infiltrated with fibrin. The brain is usually normal, but 
may be dry and firmer than usual. 

The Lungs are retracted and anaemic, the pleura may be dry or 
coated with fibrin. 

The Heart is normal. 

The Peritoneum may be dry or coated with a layer of fibrin. 

The Stomach is usually unchanged, but may be the seat of ca- 
tarrhal inflammation. 

The Small Intestine. — There may be ecchymoses in the mucous 
membrane ; the mucous membrane may be soft and oedematous : 
there may be general congestion, or the congestion ma}^ be confined 
to the peripheries of the solitary and agminatod nodules, and these 
nodules may be swollen ; or there may be croupous inflammation and 
superficial necrosis. All these changes are regularly most marked 
at tho lower end of the small intestine. There is at)t to bo post- 
mortem desquamation of the epithelium. Tlie characteristic rice- 
water fluid may be found in the intestines after death, ov instead oi 
this a dark-colored, bloody fluid. 

The Large hitestiiie is usually normal, but in some epiiloiuios 
croupous inflammation occurs in a considerable nun\ber of cases. 



210 THE INFECTIOUS DISEASES. 

The Spleen may be soft. The Liver may show sm.all areas of 
granular or fatty or hyalin degeneration. 

The Kidneys are often increased in size, with white and thick- 
ened cortex and congested pyramids. The epithehum of the cortex 
tubes may contain coarse granules and fat globules, or be necrotic. 
The tubes may contain cast matter and broken-down epithelium. 
These changes may be looked upon as being simply of a degenerative 
"character or as the results of an acute degeneration. 

The Uterus and Ovaries may be congested and contain extra- 
vasated blood. 

If the patient does not die until the stage of reaction, the body 
does not present the same collapsed appearance, and there are often 
inflammatory changes in different parts of the body, especially in the 
larynx, the lungs, the stomach, and the intestines. 

According to the researches of Koch, which have been abundant- 
ly confirmed by others, there are constantly present in the small 
intestines of cholera patients, during the early and active stages of 
the disease, characteristic curved bacilli which are not known to occur 
in the body under any other conditions, and which have been proved 



^-^feU-'A 



Fig. 9?.— Spirillum Cholera Asiatics. 
From a culture. 



to cause the disease. These bacilli are from 0.8 to 2.0 yW long, and 
are sometimes slightly, sometimes considerably curved (see Fig. 97). 
When growing, the individual bacilli are apt to chng together by 
their ends, forming S -shaped figures or spirils of considerable length. 
They are therefore often called Spirillum cholerce Asiaticce. From 
the curved shape of the individuals they are also often called " com- 
ma baciUi.'' They may be present in moderate numbers in and 
beneath the mucous membrane of the intestuie, and in very large 
numbers in the intestinal contents and in the dejections in the acute 
forms and early stages of the disease. 

In the process of their growth and multipHcation in the intestinal 
canal they apparently produce a poisonous substance, the local 
action and absorption of which into the body fluids produce the 
symptoms and lesions of the disease. The systemic effects appear 
to be in the nature of a septic intoxication. The cholera bacillus 
may retain its vitahty for a considerable period in water, and on 



THE INFECTIOUS DISEASES. 211 

moist substances, such as damp linen, earth, and vegetables, may 
increase in numbers with great rapidity. 

A temperature of from 30° to 40° C. is most favorable for their 
growth. At about 16° C. their proliferative activities cease, but 
they are not killed by —10° C. They are readily killed by dr^dng, 
and the presence of acids is very inimical to their growth. 

There is not sufficient evidence that they form spores, and their 
period of life is short. 

The cholera bacillus is readily cultivated on artificial culture 
media, such as gelatin, agar, milk, beef tea, potatoes, etc. In fluids 
it is capable of performing active movements. 

While they may be readily stained by the ordinary methods 
when present in the dejecta, their morphological characters are not 
absolutely distinctive, since several forms of curved bacilli belonging 
to the same group and closely resembling them have, under vary- 
ing conditions, been found in the dejecta and in the mouth. 

It is often of the highest importance to determine, at the earliest 
possible moment, whether or not a suspected case be one of Asi- 
atic cholera or some other form of acute intestinal disorder, so that 
the proper measures may be instituted to prevent the spread of the 
disease. The characters which are developed in the cultures of the 
cholera bacillus enable an expert biologist to distinguish this organ- 
ism from all other known forms. 

Gelatin plate cultures are made in the usual way (see page 136) 
from the intestinal contents, very small portions being taken. A 
considerable number of plates should be made, of varying dilutions, 
and kept at about 21° C. (70° F.) Usually after about twenty-four 
hours the colonies of the cholera germ appear as small, rounded, 
grayish, granular bodies with rough edges. As the colonies grow 
they become more coarsely granular, and after a time look as if 
composed of strongly refractile granules, like particles of p(mnded 
glass. The gelatin becomes fluidified around the growing colony. 
which sinks into the fluid-filled pit thus formed. In gelatin tubes 
inoculated in the usual way with the cholera bacillus, the gelatin is 
fluidified along the puncture line, but most rapidly at the surface, 
where a small air bubble usually lies at the top of the fluidified })it. 

On potatoes the cholera bacillus grows but slightly at ordinary 
temperatures, but in the thermostat, at the temperature of the bod\-. 
it grows rapidly, forming a light-grayish or brownish pellicle. 

By thus taking together the morphological and biological charac- 
ters, it is possible, usually on the second or tliird tlay, to detcnnine 
whether the intestinal contents of a suspected t-ast^ do or do not 
contain the bacillus of Asiatic cholera. 

The cholera bacillus, bv)tli iu the dejecta and iu ]>inv cultures, is 



212 THE INFECTIOUS DISEASES. 

readily stained by the ordinary anilin dyes. The results of the in- 
troduction of considerable quantities of cholera bacillus cultures 
into the gastro-intestinal canal of animals have abundantly proven 
the causative relation of the bacillus to the disease. ^ 

The disease is communicated from one person to another by the 
pollution of food or drink with the discharges which contain the 
virulent germs. 

^ For the details of his researches on Asiatic cholera, see Koch's report, "Arbeiten 
a. d. kalserlichen Gesundheitsamte," Bd. iii., 1887. 



RELAPSING FEVER. 

Synonyms. — Typhus recurrens ; Famine fever ; Spirilhim fever. 

The Skin may be jaundiced ; it may be mottled by extravasa- 
tions of blood. 

The Brain and Spinal Cord are unchanged. 

The Pharynx and Larynx may be the seat of catarrhal or croup- 
ous inflammation. 




Fir. 98.— Spiroch.;ete Obermeieri in the Blood in a Case op Relapsing F^ver. 



The Lungs. — There may be bronchitis, broncho-pneumonia, lobar 
[)neumonia, hypostatic congestic^n, and pleurisy. 

TJie Heart is often soft and flabby, Avith degeneration of its nui<- 
cular fibres. There may be ecchymoses in the pericardium. 

The Stomach, and Sniatl Litest in e may be conuvsted : tliero mav 
be ecchymoses in the mucous membrane ; there may be catarrlial in- 
flammation. 

T/te (\)foninay\)e the seat of catarrhal or ci\>up(>us iallaiuiuation. 

The 2fesenterfc Nodes may In^ swollen. 

21 



214: THE INFECTIOUS DISEASES. 

The Liver is often enlarged and the hepatic cells are swollen and 
granular. 

The Sx^leeni^ large and soft, like the spleen of typhoid fever. The 
change in its consistence is so marked that the spleen may rupture 
spontaneously during life. The spleen may also contain infarctions 
of different sizes ; some are red, some yellow, some necrotic. Those 
which are necrotic may give rise to a local or general peritonitis. 

The Kidneys show the lesions of parenchymatous degeneration. 

The Bones. — Degenerative changes in the medulla of the bones 
have been described by Ponfick. ^ 

Bacteria. — In the blood of all parts of the body during the fe- 
brile attacks may be found, in very large numbers, a long, slender 
spirillum called Spirochcete Ohermeieri. It disappears from the 
blood during the afebrile intervals. The organism is from sixteen to 
four ).i in length, and performs rapid, undulating movements (Fig. 
98). The inoculation of monkeys with the blood of relapsing-fever 
patients which contains the bacteria induces a similar disease. Pure 
cultures have not as yet been made of these bacteria, but for the 
reasons indicated, and since the organism has never been found ex- 
cept in connection with the disease, there is every reason for believ- 
ing that the Sj^irochsete Obermeieri is the cause of relapsing fever. 

lyirch. Arch., Bd. Ix., p. 153. 



SMALL-POX. 



Sniall-i30X is an acute infectious disease, especially characterized 
anatomically by an inflammation of the skin which passes through 
a series of more or less distinctive phases of papule, vesicle, pustule, 
with a final drying of the exudate and necrotic tissue constituting 
the crust. 

Various phases of the exanthem are used to designate forms of 
the disease. 

Secondary lesions are diffuse suppurative inflammation of the 
skin, inflammations of the mucous membrane, hgemorrhages in vari- 
ous parts of the body, and acute degeneration of the kidney, liver, and 
spleen. 










^^)^:^^^y-'^^F^^^^ -'fe^'^^if^^E;:^ 









■y^ 



Fig. 99.— a Small-pox Vesicle op the Skin. 



The skin lesion shows in general at first circumscribed areas of in- 
flammation above the ends of the papillse, with the development of a 
fluid-filled reticulum, so that vesicles are formed (Fig. 90). These at 
first contain a clear fluid, but by the gathering of pus cells the fluid 
becomes turbid and accumulates to form a pustule. Hand-in-haiul 
Avith these changes the papilkB and adjacent layers of the coriuiu 
may become infiltrated with cells. The contents of the pustules 
and the necrotic tissue above dry and form the crusts. When the 
t'lianges are largely confined to the epidermis the lesion may leave 
no deformity. But if the changes in the cutis are considerable, cica- 
tricial tissue may form, lea,ving scars. The association of local 
luemorrhage with the above cliangc^s gives riso t<^ tlie liaMuorrliagic 
ft>rm of exanthem. 

The micro-organ isiu causing sinall-po\: is unkm)\\'n. 



SCARLET FEVER. 

This is an infectious disease characterized by a skin eruption, 
and frequently accompanied by inflammation^ either catarrhal, croup- 
ous, or gangrenous, of the tonsils, pharynx, and larynx. 

There may be acute hyperplasia or suppuration of the cervical 
hinph nodes. There is very frequently an acute exudative or an 
acute diffuse nephritis. The spleen may be enlarged. Broncho- 
pneumonia, endocarditis, and pericarditis may occur. 

The exanthem or skin eruption in scarlatina is a simple derma- 
titis, as the result of which the papillae and subpapillary stratum 
become infiltrated with fluid or leucocytes, or both, the leucocytes 
being gathered especially about the blood vessels. There may be 
small haemorrhages, and the acute phase of the inflammation is fol- 
lowed by an increased production of epithelium and an exfoliation 
of the superficial layers. These lesions of the skin are, excepting 
the haemorrhages, very slightly marked after death. 

That the disease is due to some form of micro-organism there can 
be no doubt. The exact nature of this organism is not yet known. 
The lesion of the kidney appears to be due to some poison produced 
in the body during the disease. One of the most marked features of 
the disease is the predisposition which it entails to the incursions of 
pathogenic germs other than those which we believe to cause the dis- 
ease itself. Thus an infectious croupous inflammation in the mouth, 
tonsils, pharynx, larjmx, and trachea, due to a streptococcus (see page 
160), is a frequent complication. True diphtheria due to the Loffler 
bacillus is also prone to establish itself upon the vulnerable inflamed 
mucous membranes. So also the pneumonic and suppurative com- 
plication may be -due to a secondary infection with the pyogenic cocci. 



MEASLES. 

An intense hypersemia with inflammation of the skin, associated 
with catarrhal inflammation of the mucous membrane of the air 
passages, are the most prominent anatomical features of this infec- 
tious disease. The inflammation of the skin is anatomically of the 
same general type as that in scarlatina. Acute degeneration of the 
kidney or acute exudative nephritis may follow. The more common 
secondary lesions are broncho-pneumonia, pseudo-membranous in- 
flammation of the pharynx and larynx, suppurative inflammation 
in various parts of the body, and diphtheria. These complications, 
as in scarlatina, are doubtless, in part at least, due to secondary in- 
fection with other germs than those causing the disease itself. 

The micro-organism causing measles is not definitely known. 

Canon and Pielicke ^ have recently recorded the discovery in the 
blood in fourteen cases of measles of a very small bacillus, about as 
long as the radius of a red 'blood cell, but varying considerably in 
size. It is best stained with Czenzynski^s solution (page 68), or 
with a solution containing one-half the amount of eosin. Sometimes 
the staining is uniform, sometimes the middle portion is paler. 
These bacilli were sometimes abundant, sometimes scantv in the 
blood, lying singly or in heaps. Meagre cultures were obtained 
in three cases in beef tea. They did not seem to grow on the 
ordinary solid media. Bacilli similar in form were found in the ex- 
udate from inflamed mucous membranes in measles. The observa- 
tions of these writers are interesting and suggestive, but until they 
shall have been confirmed by others and been greatly extended 
nothing can be regarded 
significance of the germs. 



nothing can be regarded as established regarding the etiological 



1 Berliuer klin. Wochensclirift, April ISth, 1893, No. 16. 
23 



TYPHUS FEVER. 

This disease has not, so far as we know, any characteristic lesion 
save the skin eruption ; but yet after death we may find a number of 
morbid conditions, such as are common to the infectious diseases. 

The entire body has a tendency to rapid putrefaction. 

The blood is often darker and more fluid than in other diseases. 

The voluntary muscles may undergo waxy and granular degene- 
ration. 

The brain and its membranes may be congested. 

The mucous membrane of the pharynx and larynx may be the 
seat of catarrhal or croupous inflammation. 

In the lungs there may be bronchitis, broncho-pneumonia, or hy- 
postatic congestion. 

The walls of the heart may be soft and flabby. 

The agminated nodules of the ileum, and the mesenteric nodes, 
may be a little swollen. 

The spleen is often large and soft. 

The kidneys and liver are frequently the seat of parenchymatous 
degeneration. 

The nature of the infective agent in typhus is unknown. Several 
observers have recorded the flnding of micro-organisms of one kind 
or another in the disease, but proof that any of these have causative 
relationship to the disease has not yet been furnished.^ 

^ The most recent bacteriological study, that of Brannan and Cheesman, made on 
cases occurring in New York, while furnishing suggestive groundwork for future 
research, leaves the problem of its etiology still unsolved. See Brannan and 
CJieesman, " A Study of Typhus Fever," Medical Record, June 35th, 1893. 



HYDROPHOBIA. 

The lesions which have been found in this disease are not con- 
stant nor are they characteristic. Though well marked in some 
€ases, they are but very slightly developed in others. 

The lesions, when present, are apt to be most marked in the 
medulla oblongata and pons, but they may be present in the cord. 
They consist of small haemorrhages, and accumulation of leucocytes 
about the blood vessels in the perivascular lymph spaces, and of 
thrombi in the smaller blood vessels. 

While there is much reason for believing that hydrophobia is due 
io the introduction into the body of some special form of micro-or- 
ganism, and while the recent researches of Pasteur and others have 
brought to light many interesting and important facts regarding 
the general nature and distribution in the body of the infectious 
agent, nothing is yet definitely known about the particular organism 
which induces the disease. 



YELLOW FEYER. 

Kigor mortis is marked and occurs early. 

The Brain and its meninges are usually congested. 

The Skin is of a yellow color from the presence of bile pigment, 
and may be mottled by ecchymoses. 

The Heart is of a pale or brownish-yellow color. Its muscular 
fibres are the seat of fatty degeneration. 

The Lungs are congested. 

The Stomach often contains the characteristic black fluid which 
is vomited during life. Its mucous membrane is congested, soft- 
ened, and sometimes eroded. 

The Intestines are dark- colored, often distended with gas, and 
sometimes contain blood. 

The Liver in the earlier stages of the disease may be intensely 
congested. More frequently it contains but little blood, is of a light- 
yellow color, and the hepatic ceUs are infiltrated with coarse gran- 
ules and fat globules. There is in many cases necrosis of liver cells. 
The gall bladder is contracted and contains but little bile. 

The Spleen shows no marked changes. 

The Kidneys present the lesions of an intense form of paren- 
chymatous degeneration. The tubules may contain, according to 
Councilman, masses of hyalin material. 

While its mode of occurrence and the character of its symptoms 
and lesions afford a strong presumption that yellow fever is an acute 
infectious disease, none of the various studies which have been made 
upon its etiology have as yet revealed the presence of any micro-or- 
ganism to the action of which it can be fairly attributed. ^ 

' The sXndde^ of Sternlerg on.i}\e " Etiology and Prevention of Yellow Fever," pub- 
lished in the form of a Government report in 1890, contain the result of a great deal 
of research by modern methods, and should be consulted for a full exposition of this 
disease and its lesions. 



THE MALARIAL FEVERS. 

The characteristic lesions of malarial poisoning are certain 
■changes in the blood, the spleen, and the liver. 

In the more intense and acute form of malarial poisoning the 
Mood contains numerous particles of black or brown pigment, which 
are either free or embedded in cells resembling the white blood cells 
and the endothelium of the blood vessels. After death this pigment 
is found in the blood vessels throughout the body, but is most abun- 
dant in the blood vessels of the liver (see Fig. 243) and spleen. These 
organs are then usually of large size and of a peculiar brown or 
black color. 

In some of these severe cases there are also extravasations of 
blood from the mucous membranes and in their substance. There 
may also be general jaundice. 

In the milder and more protracted cases of malarial poisoning 
the composition of the blood is altered and the patient may become 
profoundly anaemic. The spleen may become the seat of chronic 
interstitial inflammation with pigmentation (see Fig. 253). The 
liver may exhibit the changes of chronic interstitial hepatitis. 

The attempts to establish a causative relationship between the 
various forms of bacteria which from time to time have been found 
in the bodies of persons who are the \actims of malarial poisoning, 
and the symptoms and lesions of the disease, have all been unsuc- 
cessful. 

On the other hand, a large number of careful studies by various 
•observers have led to a strong presumption that the disease is due, 
not to a vegetable, but to an animal organism which is very con- 
stantly found in the blood of affected persons. 

In brief, the facts upon which this presumption rests are as fol- 
lows : The blood of those suffering from malarial poisoning may 
contain one or more of the structures which are shown in Fig. 100. 

1. Inside of the red blood C(41s may bo found colorless bodies, 
sometimes occupying a small part, sometimes nearly tilling the coll. 
These bodies may or may not contain pigment granules. They may 
exhibit amoeboid movements (</ and h). They are called the (tma'- 
hold bod i en. 



222 



THE INFECTIOUS DISEASES. 



2. Colorless discoidal bodies, usually a little larger than the red 
blood cells, which contain pigment particles, sometimes scattered 
irregularly, sometimes grouped toward the centre. These are be- 
lieved by some observers to be the later developmental stages of the 
amoeboid bodies, which have increased in size at the expense of the 
red blood cells. A grouping of pigment granules indicating seg- 
mentation is sometimes seen in these bodies. These are called the 
encysted bodies (c). 

3. Bodies, about the size of a red blood cell, which are composed 
of a congeries of irregularly rounded structures grouped about a 
central mass of pigment. These are called segmenting bodies or 
rosettes (d). 







f- 





Fig. 100.— The Kematozoon of Malaria (Tlasmodium Malarle) in the Blood. 

a, tinpigmented amoeboid body in a red blood cell; b, pigmented amoeboid body; c, colorless 
discoidal body with pigment; d, segmenting body; e, fragmeots of segmenting body; / and g, 
crescentic bodies; 7i, flagellate body, a, b, d, e,f, g are drawn from specimens of malarial bloods 
prepared by Dr. Walter James; c and h are drawn after sketches by Dr. James. 



4. Smaller isolated or clustered structures which are apparently 
the result of the breaking apart of the segmenting bodies, as seen 
at e. Often called spores. 

5. Crescentic bodies containing a central mass of pigment (/ 
and g). 

6. Bodies, smaller than a red blood cell, which are actively mo- 
bile and are furnished with one or more flagella at one side — h^ 



THE INFECTIOUS DISEASES. 223 

flagellate form. These are the main forms which have heon de- 
scribed. 

The amoeboid forms are apt to occur in the acute stages of the 
disease, the crescentic forms in the chronic stages. The segmenting 
bodies are apt to be present immediately before or during the chill ; 
the pigmented amoeboid bodies, according to James, are present at 
all times, but are most numerous during and before the paroxysms. 
In general, it may be said that the number of these bodies is pro- 
portional to the gravity of the case. The amoeboid forms disap- 
pear shortly after the administration of quinine, while the crescen- 
tic bodies often persist for a considerable time under the same 
conditions. 

Whether these various bodies are developmental forms of the 
same organism or not has not yet been fully established, as artificial 
cultivations have not been made. 

The organism, which apparently belongs among the protozoa, 
may be most appropriately called the hcematozoon of malaria. It 
is, however, often called the Plasmodium malarise. 

Whatever its etiological significance or its life history, its discov- 
ery in the blood, even with our present knowledge, since it is un- 
known except in malarial disease, is of great diagnostic value in 
doubtful cases. 

Method of Examination. — The fresh blood taken from a finger 
prick may be examined in thin layers on the warm stage with one- 
twelfth oil immersion. Or the blood may be spread in a very thin 
layer on a cover glass, dried, passed through a flame, and then 
stained as in the ordinary mode of bacterial examination with f uch- 
sin or methylen blue (see page 130). The stained specimens may be 
mounted and preserved in balsam. 

By the action of Czenzyn skip's fluid, in the manner described on 
page G8, upon malarial blood, a double staining ma}- be obtained, the 
nuclei and plasmodia being stained blue while the red blood cells and 
eosinophile granules are colored red. 



TrrMOES. 



SECTIOI^ I. GENERAL CHARACTERS. 

Tumors are composed of the same types of tissue as those normally 
existing in the body, and from the latter they are derived by a pro- 
liferation of pre-existing cells. The tissues of tumors may be similar 
to those of the part in which they grow, when they are called ho- 
mologous ; or they may be dissimilar, and are then called heterolo- 
gous. Tumors are not only analogous to the normal tissues of the 
body in structure, but their life history transpires under the same 
general laws of nutrition, growth, reproduction, etc. With this im- 
portant difference, however : that while the normal, tissues, serv- 
ing as they do a definite purpose in the organism, are closely limited 
in their growth and minute characters by physical and other condi- 
tions which determine the uniform development and correlation of 
various parts, the tissues of tumors exhibit a certain lawlessness in 
growth, structure, and life history which gives them a distinctive 
character while not removing them from the physiological types. 
Thus in the Chondromata^ the tissue, while distinctly cartilaginoLis 
in t}^e, presents itself not only in places where it does not belong, 
but may show a tendency to the development of fibres in one part of 
its basement substance, while another may be distinctly hyalin* or 
another soft and almost gelatinous. The cells also are apt to ex- 
hibit great lack of uniformity in size, shape, and grouping. The 
lawlessness in tumor tissues is shown in their tendency, under cer- 
tain conditions, to change from one form into another, as from fib- 
rous tissue into bone. 

Tumors are supplied with blood vessels which grow into them 
from adjacent healthy parts, just as they do into granulation tissue, 
so that they may finally possess a more or less independent vascular 
system of arteries, capillaries, and veins. They are furnished with 
lymph vessels and some of them with nerves. The cell division by 

^ Tumors are designated by the termination oma (plural omata). 



TUMORS. 22o 

which tumors grow exhibits the same minute phenomena as does 
cell division in normal tissues (see page 72). Tumor tissues are sub- 
ject to the same degenerative changes as other tissues ; they may 
become fatty or calcified, ulcerated, gangrenous, pigmented, etc. 
By necrotic changes a tumor may be largely destroyed, but com- 
plete obliteration rarely occurs in this way. They are liable to un- 
dergo the ordinary inflammatory changes, granulation tissue may 
form in them, and abscesses and cicatrices. 

The rapidity of growth of tumors varies greatly ; some grow 
very slowly indeed and may change but imperceptibly in size and 
appearance for years, while others, on the other hand, grow so fast 
that they do not acquire solidity, and their elements remain in an 
incompletely developed condition and are thus more liable to de- 
structive changes than normal tissues are. In healthy tissues the 
blood vessels are supported by surrounding elements, which aid them 
in sustaining the blood pressure from within. In rapidly growing 
tumors this external support is often lacking, and, as the walls of 
the blood vessels are themselves badly formed, the result is that the 
walls are apt to become pouched or aneurismal, and they often burst, 
giving rise to larger or smaller interstitial haemorrhages. 

Tumors have various shapes : nodular, tuberous, fungoid, poly- 
poid, papillary, dendritic, etc. 

Tumors may occur singly or in greater or less numbers in the same 
or in different parts of the body. If they are multiple they may 
have occurred simultaneously or at different times as independent 
structures. Or multiple tumors may occur as the result of the dis- 
semination in the body, from a primary tumor, of cells which form a 
starting point for new tumors. Many tumors are sharply circum- 
scribed, may be even encapsulated, and influence surrounding parts 
only by the pressure which they exert upon them. In this way they 
may cause displacement, atrophy, or necrosis ; they may, by pressure 
on neighboring vessels, cause oedema, thrombosis, etc. ; they may in 
the same way cause dislocation and caries of bones. 

Tumors may grow largely by increase of elements within them, 
thus simply expanding ; this is called cenfi-aJ (ji-oirfh. They may 
grow in part or largely at the surface — peripheral ijroirth. In this 
case the growth may be a direct, continuous enlargement of the mass 
at or near the periphery, or it may be by the formation of secondary 
nodules near the primary growth, Avliich, gradually enlarging, finally 
coalesce with the latter, fonning a part of the nodular tumor. This 
mode of enlargement is called diseonii)iuous peripheral (jrairfh, 
and is due to the dissemination of cells from the mother tumor into 
the adjacent tissue through the blood or lymph channels, and tlieir 
proliferation at the points of lodgment. This dissemination may 



226 TUMORS. 

occur by the agency of blood or lymph currents or by the amoeboid 
movements of the cells. 

It is not yet certain whether the new cells which are produced in 
tumors are altogether the result of the proliferation of the primary 
tumor cells, or whether the ordinary tissue cells of the part, connec- 
tive-tissue cells, white blood cells, etc. , may undergo transformation- 
and proliferation under the influence of the characteristic cells of the 
tumor. It is not unlikely that both modes of increase occur, although 
the former is probably the more common and important. Some 
tumors increase by an infiltration of surrounding tissues, whose ele- 
ments they gradually replace. In certain tumors the old tissue of 
the part in which they grow may remain T\T.th its vessels and form a 
sort of matrix whose interstices are infiltrated with the new tumor 
tissue. The irritation of the tumor may induce inflammatory new 
formation of tissue of the old matrix about or within the tumor. 

But all tumors are not limited to that part or region of the bod^r 
in which they first occur. Sooner or later secondary nodules re- 
sembling the first may be found in the most distant parts of the 
body, sometimes singly, sometimes in great numbers. These may 
grow like the parent tumor, and themselves form foci for new dis- 
seminations. 

This dissemination of tumors is one of the most important ele- 
ments of malignancy, and is called metastasis, the secondary tumors 
being called metastatic tumors. This occurs by the transportation. 
of tumor cells through the blood or lymph channels. Since the 
tumor itself may be filled with new and badly formed blood and 
lymph vessels, and its structures be in close contact ^vith the vessels 
of the tissue in which it grows, the cells of the primary tumor may, 
by ulceration through, or by atrophy of, the walls, readily find their 
Tvay into the lumen of the A^essels and be swept away by currents as. 
emboli, and, finding lodgment, proliferate and grow, forming sec- 
ondary tumors; or the proliferation may occur in the vascular endo- 
thelium itself, when the formation of emboli is easv to understand.. 
When carried through the lymph vessels the tumor cells may for 
some time be kept from the larger channels and from general dissemi- 
nation by lodgment in the hTuph nodes, where they may establish 
independent tumors. The parts of the body in which metastatic tu- 
mors are most apt to form depend, of course, upon the situation of the 
primary tumor and the distribution of the vascular channels through 
which dissemination occurs. 

The tumors in which metastasis is most apt to occur are, as a 
rule, those which grow rapidly, are vascular and succulent, and con- 
tain many cells. 

Not less variable than the size, mode of growth, and structure of 



TUMORS. 227 

tumors is their significance in the organism. Surgeons have in the 
past, and to a certain extent still do classify tumors, for practical 
purposes, as malignant and benign, and for a long time malignant 
tumor and carcinoma were synonymous terms. Now we know that 
other tumors as well as carcinomata are malignant, and, furthermore, 
contrary to the former belief, that malignancy does not depend upon 
any specific extra-cellular agent in the tumor. If we mean by a 
malignant tumor one which may cause death, any tumor may be 
malignant if growing in the right place. Thus a simple fat tumor, 
by pressing on the trachea, may cause suffocation, and any tumor 
may secondarily cause death by haemorrhage or septicsemia. The 
real signs of malignancy in a tumor are: 1. Invasion of adjacent 
tissues by eccentric or peripheral growth. 2. The tendency to local 
recurrence after removal. 3. The formation of metastases, -i. A 
tendency to interfere with the nutrition and general well-being of 
the body, which may give rise to a condition known as cachexia. 
The modes of invasion of surrounding tissues and the formation of 
metastases have been considered above. The tendency to local re- 
currence after removal is probably, in most if not all cases, due to 
the incomplete removal of the peripheral infiltrating cells. These 
may be very few in number and lacking in characteristic structural 
features, but are none the less endowed with the capacity of prolifera- 
tion and development into a new and similar tumor at or near the 
seat of the extirpated one. The infiltrating peripheral cells may re- 
main dormant for a long time after an operation, or may imme- 
diately commence to grow. The mere fact that a second tumor de- 
velops in the place of one removed does not imply malignancy, since 
it may result from the same mechanical cause which produced the 
first, as in the case of certain carcinomata of the lip induced by the 
mechanical irritation of a pipe. 

The drain upon the system by the rapid growth of a tumor, to- 
gether with the absorption from it into the bcxlj^ of deleterious putre- 
factive materials, from sloughing, ulceration, and degeneration, may 
give rise to fever and other constitutional disturbances. Or thov 
may induce feebleness, anaemia, and that general impairment of the 
nutritive functions of the bod}^ known as cachexia. This condition 
is frequently rendered worse by the mental status of the jKitient in 
the presence of such a traditional object of alarm. 

It should be remembered, however, that so louii- as thevaro local- 
ized and have not undergone degenerative changes, even the most 
malignant tumors do not usually give rise to a cachexia, since the 
drain upon the nutritive powers of the systcMu by their simple growth 
is not, under ordinary conditions, very consiilerable. AVheu the 
system is deteriorated by the absorj)tion of sceptic materials from 



.228 TUMORS. 

tissue degeneration, however, this may become a very important 
factor. 

This condition of cachexia, so evidently secondary to the growth 
and degeneration of the tumor, was formerly termed a dyscrasia or 
diathesis, and was supposed to precede and induce the growth of 
.malignant tumors, particularly cancers. 

It is further to be noted that the fragments of tumors which have 
found access to the veins may act as simple emboli and produce im- 
mediate death or simple metastatic abscesses. 

It was formerly supposed, when the doctrine of the specific nature 
of tumors prevailed, that the cells of malignant tumors, particularly 
of carcinomata, had a characteristic structure and appearance, and 
that by the examination of single or of a few separated cells the na- 
ture of the tumor could be determined. From the above considera- 
tions it will be evident, as all tumor cells have their prototypes in 
the normal body, that therefore there is nothing pathognomonic in 
the appearances of single cells. It is by a study of the general struc- 
ture and of the topography of tumors, as well as of the characters 
of the individual cells, that we are enabled to determine their nature. 
And even then we must often bring to our aid the clinical history and 
gross appearances of the growth before we can arrive at a definite 
conclusion. We may, indeed, sometimes, aided by the clinical his- 
tory or gross appearances, be able, by the microscopical examination 
of scrapings from a tumor or of fluids from an internal cavity in 
which it is growing, to form a reasonable conjecture regarding its 
nature. 

As a rule, the peripheral portions of the more rapidly growing 
"tumors are best adapted for microscopical examination, because here 
secondary degenerative changes are less likely to have occurred than 
in the central parts. 

THE CAUSE OF TUMORS. 

In regard to the causation of tumors our actual knowledge is still 
^ery meagre. In a certain number of cases mechanical influences 
.are undoubtedly sufficient inciting causes. In other instances hered- 
ity is an important factor. But to both of these influences too much 
importance has been attributed in former times. The most recent, 
.and to a certain extent plausible, hypothesis, and one which most sat- 
isfactorily accounts for the occurrence and character of many tu- 
mors, is that of Cohnheim, called the hypothesis of the embryonal 
origin of tumors. This is to the effect that all true tumors are due 
to faulty embryonal development ; that certain embryonal cells of 
various kinds, in the course of the development of the body, are 



TUMORS. 229 

superfluous, or become displaced, or do not undergo the normal chan- 
ges, and remain ready, when the conditions shall become favorable 
in later life, from whatever reason, to commence growing with all 
the potencies of embryonic and lowly organized cells in the midst of 
the mature tissues. ISTot being restrained, however, by the regulat- 
ing influences which determine the nature and relative extent of 
growth in normal development, they go on to the production of tu- 
mors, which represent, though in atypical form, the various tissues 
which the strayed or unused cells were destined normally to pro- 
duce. 

The evident hereditary character of many tumors, the congenital 
nature and early development of others, their atypical structure in 
general, and the tendency of many forms to occur in situations in 
which, during the development of the embryo, considerable com- 
plexity exists, as well as their heterologous occurrence and their fre- 
quent primary multiplicity — all of these characters of tumors seem 
to favor Cohnheim's hypothesis. On the other hand, the theory 
leaves unexplained the sudden growth of the alleged embryonal cells 
which have long remained dormant, and lacks as yet the absolute 
demonstration of a morphological basis, since no one has seen the 
strayed or delayed embryonic cells. These may, of course, be very 
small and difficult of demonstration, and this, according to Cohn- 
heim, fully explains the lack of a definite histological basis to his 
hypothesis. It should be remembered, furthermore, that, under or- 
dinary conditions in the body, certain cells which are destined to 
replace others which have fulfilled their destinies, as in the skin, pos- 
sess to a greater or less degree the characters of embryonal cells, 
and that while in the struggle for existence the growth of these cells 
may be held in check, as by conditions of pressure, nutritive supply, 
etc., if these conditions be altered these cells may undergo prolifera- 
tive changes as significant as those of the alleged belated germs of 
Cohnheim. Such a changed condition of affairs has been shown by 
Thiersch to occur frequently in the skin in old age, and to explain 
in large measure the occurrence of certain epithelial tumors. It 
should be remembered that this In^pothesis was offered by Cohn- 
heim only as a suggestion to facilitate research, and that he ex- 
pressly warned his confreres against attaching a premature inqun-- 
tance to the possibility to which ho called attention. Thus, while the 
hypothesis of the embr3"onal origin of tumors is most fascinating, 
and for certain forms quite satisfactory, we may well demand a 
more definite basis of fact before accepting it as of iinivei*sal a[>pli- 
cation. 

Bacteria have in recent times been claimed by some obsorvors to 
stand in a causative relation to certain tumors, and bacteria have 



'^30 TUMORS. 

iDeen occasionally demonstrated in, and cultivated from, the tissues 
of tumors. But no complete and reliable experiments or observa- 
tions have as yet been made which prove that they have anything to 
do in causing the tumors, or are of any significance save as chance 
contaminations of the tissues or as inducmg secondary complications. 
A great deal has recently been written — in view of the more or 
less plausible notion that tumors might be of parasitic origin — about 
certain structures which are not infrequently found mostly in, but 
sometimes between, tumor cells, especially in the carcinomata, and 
which have been rather hastily assumed to be animal or vegetable 
parasites. These cell *"' inclusions "^ are for the most part larger or 
ismaller rounded bodies (Fig. 101); with or without nuclei; sometimes 
mth double contours, sometimes not; usually sharply outlined against 












W^i^ 






m 




^'^i^^,'!f-^"' ■"■"'**iiv.: 



Fig. 101.— Epitheliai, Cell "Inclusions" in Tumors. 
Showing various forms. From carcinoma. 

"the cell protoplasm in which they lie; often crowding the cell nucleus 
to one side, often situated within the nucleus, often apparently re- 
placing it. These structures seem to be invaginated epithelial or 
other cells, or cell nuclei which have undergone various degenerative 
"metamorphoses, fragmentation, etc. In some vacuoles are developed ; 
some he in vacuoles in the tumor cells. They may be single or there 
may be several in a single tumor cell. Some of the questionable 
.structures appear to be the metamorphosed nuclei of the tumor cells 
themselves. 

They are found in other than tumor tissues. 

These protean structures are no doubt of varied origin, and have 
b)een most frequently thought of late to belong among the cocci- 
•dia. They are readily stained with varying degrees of intensity by 



TUMORS. 231 

licematoxylin, by eosin, by saf ranin, or by f uchsin. ' Some of the cell 
inclusions in carcinoma may be coccidia or allied organisms. 

We do not, of course, assert that tumors cannot be caused by 
parasites, but at present it seems to us that no adequate ground 
exists for believing that they are. 

The nearly uniform failure of success in the transplantation of 
tumors from one species of animal to another, and the absolute failure 
to cultivate, either directly or by inoculation, any constant organisms 
from them, speak with much force against the notion of the parasitic 
origin of malignant tumors. 

It seems to the writer that to seek for a single external cause or 
group of causes for the aberrant tissue growths which we call tumors, 
is to ignore the many still obscure inherent influences Avhich are at 
work in all tissue growth, especially those influences which foster 
simple cell proliferation and tend, under the influence of heredity, to 
specialization in form or function. On the other hand, not to be 
ignored are those influences, whether of nutrition or pressure or ex- 
posure, which mould the cell growth under normal conditions into 
purposeful and fixed forms. 

It is rather a matter of surprise that ever-changing, self- regenerat- 
ing living tissue does not of tener go astray in its activities than that 
it only now and then should do so. This latter somewhat inverted 
point of view may be useful in calling away the attention, in dis- 
cussing the etiology of tumors, from a too close regard to extraneous 
factors, and directing it to the many still unexplored fields in cell 
physiology which we must perhaps become familiar ^^^th before we 
can, with fair hope of success, attack the problems, both in cause 
and cure, which crowd thickly about these significant tissue aberran- 
cies — the tumors. 

CLASSIFICATION OF TUMORS. 

The fact that tumors are composed of structures which resemble 
the various types of tissue found in the normal body suggests the 
guiding principle in their classification. But in order to thoroughly 
understand either the classification of normal tissues or the grouping 
of the tumors, we must keep in mind the way in which the tissues 
.are developed in the embryo. 

According to the more recent views of embryologists, particularly 
of His and Waldeyer, the primitive tissues of the body belong to 
two groups: those of a/'(7///>/(i'.s'//V and those of /)(r/'(r/>/(T.s'//V origin. 
In the early stages of fa>tal development the nou' colls which are 

^ For bibliography and new observations consult Flcrncr, Johns Hopkins Hospital 
Bulletin, May, 1893; anil Podici/sso:/i-i and Saicfttc/wnko, Centralblatt fur Baktorioloirio, 
Bd. xi., Nos. 16, 17, 18, 1893. 



232 TUMORS. 

formed at first arrange themselves in three layers, to which collec- 
tively the name arcliihlast is applied. 

Of these three archiblastic layers, the outer, called the epihlast^ 
furnishes the material for the epithelium of the skin and its adnexa, 
for the epithelium of the terminal portions of the alimentary canal, 
and for the nervous system, including the neuroglia. 

The middle layer — the inesoblast — furnishes the material for the 
epithelium of the genito-urinary organs, and for both the smooth 
and striated muscle tissue. 

The inner layer — the liypohlast — affords the material for the de- 
velopment of the epithelium of the respiratory and the digestive sys- 
tems, with that of the various glands and passages which develop 
out of and in connection "with them. 

The exact origin of the parablast, which develops later than the 
archiblast, is still uncertain ; but it furnishes the material out of 
which are formed the connective tissues, including cartilage, bone, 
teeth, and fat ; the blood cells and blood vessels ; the Ijanphatic tis- 
sues and lymph vessels ; and the true endothelial cells. 

]Srow:, if we wish to arrange in groups the different kinds of tu- 
mors found in the body, we have only to recall the varieties of tissue 
which normally exist there, and their grouping, and upon the classi- 
fication of the physiological types to construct the classification of 
tumors. It should be remembered that the usual separation of the 
normal tissues into groups is useful, rather because it facilitates their 
study than because it expresses absolute and fundamental distinc- 
tions ; and the same may be said of all the classifications of tumors. 
In both, an increase of our knowledge concerning their structure 
and genesis will doubtless lead to a more accurate grouping : but, 
for the present, such an arrangement as that indicated below mil be 
found of practical value for the purpose of studjdng tumors. 

I. Tumors composed of Tissues of the Type of those forming 

the Connective-Tissue Group. — - 
Histioid or Connective-Tissue Tumors. 

Physiological Type. Tumors. 

1. Fibrillar connective tissue. 1, Fibroma. 

2. jMucous tissue. 2. Myxoma. 

3. Embryonal connective tissue. 3. Sarcoma. 

4. Endothelial cells. 4. Endothelioma. 

5. Fat tissue. 5. Lipoma. 

6. Cartilage. 6. Chondroma. 

7. Bone. 7. Osteoma. 

8. Neuroglia.^ 8. Glioma. 

^ It will be seen, from the account given above of the origin of the various tissues 
in the difEerent embryonic layers, that the neuroglia has a different origin from the 



TUMORS. . 2o 



o 



II. Tmnor.s coiuijostd of Tissues of the Type of Muscle Tissue. 

— Myomata. 

Physiolofjical Type. Tumors. 

1. Smooth muscle tissue. 1. Leiomyoma. 

2. Striated muscle tissue. 3. Rhabdomyoma. 

III. Tumors composed of Nerve Tissue. — Neuromata. 

Physiological Type. ' Turaors. 

1. Nerve tissue. 1. Neuroma. 

IV. Tumors composed of Vascular Tissue. — Angiomata. 

Physiological Type. T amors. 

1. Blood vessels. 1. Angioma. 

2. Lymph vessels. 2. Lymphangioma. 

T^. Tumors in 'which the Predominant or Characteristic Elements 

are Epithelicd Cells. 



Physiological Type. 


Tumors. 


1. Glands. 


1. Adenoma. 


2. Various forms of epithelial cells 


2. Carcinoma. 


and associated tissues. 





VI. Tumors formed hy Various Combinations of the above 

Types. — Mixed Tumors. 

Aside from the above well-marked classes, we may mention here 
for the sake of completeness : 

(a) Complex Congenital Tumors — Teratomata. — These are con- 
genital tumors which frequently contain a great number of different 
forms of tissue, such as various forms of fibrillar connective tissue, 
cartilage, bone, teeth, hair, skin, muscle, and glands. They are 
most fre({uently found at the lower end of the spine, about the head 
and neck, or in the generative organs. Some of them probably arise 
by an inclusion of portions of another foetus. These are called tera- 
toid tumors, or teratomata. Among them are sometimes classed 
other and simpler congenital formations, such as dermoid cysts, con- 
genital angiomata, and the so-called i)igmented moles. 

(b) Cysts. — These structures, for the sake of convenience, are 
usually classed among the true tumors, although in general charac- 
ters, structure, and genesis tlu\v are of iMitindy difterout nature. 
They are usually divided into two classes : 

I. C^ysts u'liirh derelop in pre-cvisfiug car Hies. 
TT. Cysfs which originate iudepeudeutly as the result of fmtho- 
ioyical chauijes. 

other connective tissues. The neuroglia, as well as the tumors derived fri>m it. pre- 
sents marked peculiarities in structure, but its structural aiui functional alliance \\'\\\\ 
the other connective tissues justifies its grouping among them. 

23 



234 TUMORS. 

I. Cysts which develop in pre-existing cavities : 

1. Retention Cysts, — These are chiefly formed b}^ the accumula- 
tion in glands or their excretory ducts of the more or less altered 
secretion of the gland. They usually occur as the result of some 
hindrance to the normal discharge, as from inflammatory contrac- 
tions, pressure, etc. The contents of such cysts are usually mucous, 
sebaceous, serous, or of a mixed character. Their walls are the 
more or less altered walls of the original structure. To this class 
belong comedones, milium, atheroma, chalazion, ranula, the ovula 
[N'abothi, milk cysts, and certain serous cysts of the ovaries, Fallo- 
l^ian tubes, gall ducts, and uriniferous tubules. 

2. Exudation Cysts. — These arise usually, though not always, 
as the result of a chronic inflammatory process in lymph spaces or 
serous sacs, and among them are to be classed the so-called gan- 
glia, hydrocele, etc. Certain of the so-called hsematoceles, in which 
blood is extra vasated into closed cavities, form a variety of the cysts 
of this group. 

II. Cysts which originate independently as the result of patho- 
logical changes : 

1. Cysts formed by the softening and disintegration of tissue. 
— Such cysts may at first be small and have very meagre contents and 
no well-defined wall. A wall may finally be present either as an en- 
tirely new-formed structure, or the more or less modified capsule of 
the organ in which they occur may partly or entirely form the wall. 
The contents (rf such cysts are usually the more or less altered de- 
tritus of the tissue by whose disintegration they are formed. Such 
cysts are very apt to occur within true tumors, particularly those 
which are succulent and of rapid growth, since these, as above 
stated, are very liable to degeneration. Old abscesses may change 
into well-defined cysts of this kind. 

2. Cysts formed around foreign bodies. — The inflammatory 
reaction induced by the presence of foreign bodies of various kinds, 
parasites, masses of extravasated blood, etc. , frequently results in the 
formation of well-defined encapsulated cysts. 

3. Cysts formed by a neiv groivth of tissue in ivliose spaces 
various kinds of fluid accumulate. — These spaces may or may 
not be lined with epithelium and have something of the glandular 
character. Such forms are exemplified in some of the compound 
ovarian cysts — the so-called ovarian cystomata. 

4. Congenital Cysts. — These are of various forms, and their 
mode of origin is in most cases but imperfectly understood. The 
so-called dermoid cysts of the subcutaneous tissue and ovary are 
marked examples of this class. Certain congenital cysts of the kid- 
ney and other internal organs are convenienth' grouped in this 



TUMORS. 2-'}0 

class, although it is quite probable that some of them at least origi- 
nate during fVjetal life in one or (jther of the above-described ways, 
and hence are not essentially different in nature from some of the 
cysts of other classes. For the mode of formation of certain cysts c>f 
the neck see page 446. 

Various Lesions sometimes described as Tumors. — There are 
certain enlargements of the lymph nodes which are in reality hyper- 
plasias, sometimes inflammatory in character and sometimes not, 
and which are often grouped among the tumors as lyinjjhomata. 
They are not, strictly speaking, true tumors, and will be considered 
under the lesions of the lymph nodes. 

In the same group are often classed the enlargements of the 
lymph nodes in leukaemia and in other general diseases, which will 
be treated in another part of this book. Another group of tumors 
sometimes called lymphomata are in reality sarcomata, and these 
will be described under the latter heading. 

There is also a group of nodular new formations, the so-called Iii- 
fective Granulomata, which are sometimes classed among the tu- 
mors. These are found in tuberculosis, leprosy, syphilis, lupus, 
glanders, and actinomycosis. They seem, however, to be more 
closely allied to inflammatory new formations than to true tumors, 
and, as our knowledge regarding them increases, have one by one 
been proven to be dependent upon the irritation caused by the pre- 
sence of vegetable parasites (see section devoted to Infectious Dis- 
eases). In the case of syphilis the absolute proof is still lacking. 

Nomenclature of Complex Tumors. — The simple occurrence of 
more than one kind of tissue in a tumor does not make it a com])lex 
or mixed tumor. It is only when a special kind of tissue occurs in 
sufficient quantity to be of definite significance, or is of such a 
nature as to render its presence, in any amount, of importance, that 
we recognize, its presence in the name. The name of mixed tumm-s 
is usually formed by joining the names of the tissues to be recog- 
nized. Tims a combination of fibroma and sarcoma is calknl fibro- 
sarcoma ; the general rule of constructicni being that the name of 
the more important tissue shall serve as the substantive which that 
of the less important one (qualifies. It should be remembered, how- 
ever, that the more important tissue is nc^t always the one which is 
present in greatest amount. Thus, owing to the great clinical sii;- 
nificance of carcinomatous tissue, a very large fibroma with a small 
quantity of cancer tissue intermingled would be a Jihro-Ciircinonia 
and not a carcino-fibroma. 

Preservation. — In general, tunu>rs, like all tissues for luieroseopieal stiulv, shouUl 
be cut into small pieces before immersing them in the preservative tinids, ami the 
sooner they ean be placed in these after removal the better will be the preserva- 



236 TUMORS. 

tion. In some cases much may be learned from large sections of tumors together 
with their surrounding tissues. In this case the proper part of the tumor must 
be preserved whole, and is best hardened in strong alcohol. For the ordinary 
routine hardening of tumors MilUer's fluid is probably the best agent, the harden- 
ing being completed in the usual way with alcohol. In many cases an interstitial 
injection of Flemming's solution, and subsequent immersion in alcohol, secures a 
very perfect preservation of the cells. 

When it is desired to study the living cells of tumors — and much may be learned 
in this way — fragments should be teased in one-half-per-cent salt solution and ex- 
amined on a warm stage. For purposes of immediate diagnosis, sections may be 
made of the frozen tissue and stained with safranin. For the method of obtaining 
extremely thin sections of tumor cells see page 49. 



SECTION II. SPECIAL FORMS OF TUMORS. 

FIBROMA. 

The fibromata are composed of fibrillar connective tissue, which, 
as in the physiological type, is sometimes dense and firm, Fibroma, 
darum, and sometimes loose in texture and soft. Fibroma molle. 
They are usually sharply circumscribed and are frequently encapsu- 
lated, but they may be diffuse and merge imperceptibly into the sur- 
rounding tissue. Some fibromata consist almost entirely of inter- 
cellular substance, containing but few flattened or spindle-shaped 
cells (Fig. 102) ; others contain very many variously shaped cells. 
The cells are often more abundant in one part of the tumor than in 

— ' * .p' 










Fig. 102.— Dense Fibroma of Abdominal Watx— Fibroma dcrum. 
Some of the bands of connective-tissue fibres are cut across, others are cut lengthwise. 

another. The denser varieties usually contain but few blood vessels, 
although they are occasionally <|uite vascular. Many of the softer 
varieties are very vascular. Nerves also are occasionally seen. The 
course and arrangement of the fibres in these tumors are usually 
(juite irregular, often crossing .and interlacing in a most complex- 
manner. The fibromata are usually of slow growth, but exceptii^n- 
ally they grow very rapidly. They are benign tumors, but by pres- 
sure on important organs, by ul(Hn'atit)n, (U* by changing into other 
varieties of tissue, tlu\v may become of serious imptu-t. Viirt^ til)ro- 
mata do not form nu^tastasc^s, but they are often multiple. ;uul when 
so are frecpiently congtMiital. 

It seems probable that in the nudti[)le tibrouiata of the skin ( Fibro- 
ma niolliLscui))) tlie new growths occur in some special \'ov^)\ of 



23S TUMORS. 

connective tissue, as that of the nerves, blood vessels, or glands. 
Some of these multiple fibromata are classed among the neuromata* 

While the fibromata are more commonly nodular in form, when 
they develop on the skin or mucous membranes they frequently form 
papillary outgrowths covered more or less thickly with epithelium, 
and are then called jjajDiUo mat a (Fig. 103). Common warts of the 
skin are papillomata with excessive production of surface epithelium. 
To the papillomata also belong some of the so-called condylomata. 

Fibromata may, like most tumors, exhibit local recurrence when 
not fully removed. They are frequently very small and insignificant, 
but, on the other hand, may grow to an enormous size. 






k. 



^rV•^ 













4y^i\jK 








■-" f"^^'- ': J- \ ^--^t 








^^::y'j^!}^£^'=A^ 






V 


'■ 1 --•* ' ■ " ' "'^s 






i 




..k 




\ 






.'-— ■^.^■^^ 


-1 


J^T/ --' '>-'-.\ ' 




;^'"^?^>. 


\ 






,?i 








X ._ y^ 


■ \ 1 




t "■ •' '. ' - 


■.'^^'i 




Fig. 103— Small Papilloma of the Sktn. 

They are quite frequently combined with other kinds of tissue to 
form complex tumors. The looser, softer varieties not infrequently 
become oedematous, when they may closely resemble myxomata. 
They are liable to calcification and to fatty and mucous degenera- 
tion. By metaplasia they may partially change to form fibro-chon- 
droma, fibro-lipoma, fibro-sarcoma, or fibro-osteoma. The latter 
transformation frequently occurs when they form in the periosteum. 
Developing, as they do, in the connective tissue, they occur in the 
most various parts of the body : in the skin and subcutaneous tissue ; 
in intermuscular tissue and fasciae ; in periosteum ; in the nerve 
sheaths and intrafascicular connective tissue : in the dura mater, the 



TUMOKS. 



2'6i) 



interstitial tissue of organs, and in the mucous membranes. Many 
of the so-called polypi of the mucous membranes (see Fig. lOG) and 
some psammomata are forms of fibroma, the former often approach- 
ing the myxomata in type. 

' Occasionally, in the ducts of glands, fibrous polypi grow to an 
enormous extent, their epithelial covering keeping pace in growth 
with their development, until they form very large, irregular, loose- 
textured tumors, which often finally ulcerate. Such forms are seen 
in the mammary gland, where they are frequently mistaken for car- 
cinomata. They are called Intracanalicular Fibromata (see Tu- 
mors of the Mamma). It is often difficult to distinguish between 
genuine fibromata and inflammatory or other connective- tissue hy- 




FiG, 104.— Myxoma of Subcutaneous Tissue of Back. 

perplasias, such as elephantiasis ; and perhaps the fuller knowledge of 
the future will show that the distinctions are not as definite as we 
are now disposed to believe. 



MYXOMA. 

Mucous tissue. is essentially an embrvoni(^ tissue, for in the normal 
adult it is present only in a very imperioct and atypical form in tlie 
vitreous of the eye, and perhaps exceptionally in small an^nint alnnit 
the heart, kidneys, and mtMluUa of bone. 

The myxomata are thus essentially embryonic-tissue tumors. 
These tumors consist, in their most typical forms, of a homogeneous 
ov finely fibrillated, soft, gelatinous basement substance, in which aiv 
emb(Hld(Hl a, variable numiuM' o( splieroidal, fusift^nn. branching, and 
often anastomosing c(^lls (Fig. UVl). Tlu\v may contain lew or many 



240 ^ TUMORS. 

blood vessels and nerves. By the addition of acetic acid, mucin may 
be precipitated from the basement substance. In sections it is fre- 
quently stained with haematoxylin. The very soft forms which con- 
tain comparatively few cells and much translucent basement sub- 
stance are called Myxoma gelatinosum or J/. moUe. The presence 
of many cells renders them more consistent and gives them a whiter 
and more opaque appearance ; such forms are called J/, medullare. 
Pure myxomata are not very common. The myxomata are very 
apt to be combined with fibrillar connective tissue sls fib ro- myxoma ; 
or with fat tissue, lipo-myxoma ; and they very frequently become 
sarcomatous, or take part in the formation of very complex tumors. 
They may be diffuse or encapsulated with fibrillar connective tissue ; 
they are frequently very large, and may be multiple. Owing to the 
character of the basement substance, the blood vessels not infrequent- 
ly rupture, giving rise to larger or smaller hsemorrhages within the 










Fig. 105.— Myxoma growing into Abdominal Cavity. 
Showing the accumulation of fat droplets in some of the cell bodies. 

tumor, or to the formation of cysts. The cells are liable to undergo 
fatty degeneration (Fig. 105). 

Composed, as they are, of a type of tissue from which fat tissue is 
developed in the embryo, the relations of these tumors to fat tissue 
are very intimate. They are most f requenth^ developed in. and prob- 
ably directly from, fat tissue, and are very often combined with it 
as lipo-myxoma. They are also found in the subcutaneous, submu- 
cous, and subserous tissue, in the marrow and periosteum ; in the 
brain and cord ; in the sheaths and intraf ascicular tissue of peripheral 
nerves ; in intermuscular septa ; and in the interstitial tissue of 
glands, such as the mamma and parotid. The myxomata are in 
general benign ; yet they are very prone, especially the lipomatous 
forms, to local recurrence. They sometimes grow very rapidly, and 
sometimes, though very rarely, form metastases. In the not infre- 
quent combination with sarcoma they may exhibit the most marked 



TUMORS. 



241 



malignancy. Many of the polypi of mucous membranes are myxo- 
mata or fibro-myxomata (Fig. 106), and to this class of growths be- 
long the so-called hydatid moles which sometimes develop in the villi 
of the chorion. 

QEdematous, loose, and cellular forms of fibrillar connective tissue 
so closely resemble some of the forms of mucous tissue that certain 
observers consider them as identical. So prone are many tumors to 
undergo mucous degeneration, and so frequent are the combinations 
of the myxomata with other forms of tumors, that it is often diffi- 




FiG. 106.— Mucous Polyp of the Nose. 

The section shows the epithelial covering of the new growth, as well as its numerous blood 
vessels and a few mucous glands. 

cult, sometimes impossible, to say whether the mucous tissue in a 
given composite tumor is primarj^ or secondary. 



SARCo:\rA. 

Tliese tumors are formed on the tyi)o of connective tissue, but 
they are, as a rule, largely composed of cells : the basement sub- 
stance, though a constant and important factor, being nuich less 
conspicuous than in adult connective tissue. Tlu\v more closely re- 
semble, in general, the develo})ing connective tissue of theombryi>or 
the granulation tissue of intiammation. They are, therefore, con- 
veniently described as presenting the type o\' embryonal tissue. The 
prominent and characteristic cells of the sarcomat:i are most varied 



212 TUMORS. 

in size and shape. Tliej' may be fusiform or spindle-shaped, sphe- 
roidal or branched ; thev mav be multinuclear and verv lars-e. or they 
may be very small and spheroidal, resembling leucocytes. The fibril- 
lar basement substance may be present in such small quantity as to 
entirely escape a superficial observation, covered as it may be by the 
abundant cells : or it may be so abundant as to give the tumor the 
general appearance of a fibroma. It may be intimately intermingled 
^vith the cells in fascicles, or it may be in large open-meshed net- 
works, giving to the tumor an alveolar appearance. The cells, how- 
ever, always stand in an intimate relationship to the basement 
substance, which they sometimes reveal by fibrillar processes con- 
tinuous ^\dth it. Blood vessels also form a constant and important 
structural element in these tumors, being in some of them so pre- 
dominating a factor that they give structural outline and general 
character to the growth. They, too, as in the normal connective tis- 
sue, are intimately associated with the basement substance and with 
the tumor cells. 

A single form of cells is often so predominant as to furnish a suit- 
able qualif ^'ing name for the tumor, but in many cases the cell form 
varies greatly in the same growth. It may be said, in general, that 
there is a tendency to reproduce in these tumors some of the special 
characteristics of the tissues in which they originate. Thus, sarco- 
mata of the bones are apt to be osteo-sarcomata : those of pigmented 
tissue, hke the choroid, are apt to be pigmented sarcomata. It ^\all be 
more convenient for our present i3ur]3ose to briefly describe the more 
common forms one after another than to attempt any systematic 
classification of them. 

It should be remembered, however, that the various forms are 
not sharjDly specific in character, but are apt to merge into one another 
and to intermingle in various ways. 

Sarcomata are most frequently found in the skin, subcutaneous 
tissue, fascice, subserous connective tissue, the marrow or periosteum, 
and in the choroid. They may also occur, though more rarely, in 
the dura. mater ; brain and cord ; lymph nodes : in the adventitia of 
blood vessels, and in nerve sheaths : in submucous tissue : in the ute- 
rus and ovar}^, and in the kidney. In the liver and lungs and heart 
they may occur by metastasis. 

They are more apt to occur at an early period in life than later. 
The cellular character, the rapid growth, the vascularity and succu- 
lence of many forms, the marked tendency to local recurrence, and 
the formation of metastases, stamp the sarcomata as malignant tu- 
mors. But in this they vary greatly : while some of the forms be- 
long in every sense to the most malignant of tumors, others gro^v 
slowly, are very dense, and may remain localized and harmless for 



TUMORS. 



24:} 



years. Their tendencies in tliis respe(.-t will 1x5 mentioned und(;r t\w 
special forms. 

Intimately related as they are to the hlood vessels, metastasis is 
more apt to occur through the blood than through the lymph chan- 
nels, and consequently adjacent lymph nodes are much less apt to 
be involved than in some other forms of tumor, notably the carcino- 
mata. 




Fig. 107.— Large Spindle-celled Sarcoma of Humerus. 



The richly cellular and vascular forms of sarcoma are especially 
prone to haemorrhages, degeneration, and ulceration. 

Spindle-celled Sarcoma. — The cells in these tumors may be large 
— large spindle-celled S. (Fig. 107) ; or they may be small — small 




Fig. 108.— Smat,l Spindle- celled Sarcoma op Forearm. 



spiHdle-eelled S. (Fig. H)S). Thov may consist largely ot" colls, or may 
(HUitain so much intercellular librous tissue as to be appropriately 
vnWcd fibrosa rroiK a. The cells are freipiently arranged in fasciclt^s, 
which surround thi^ blood vessels, and tliese fascicles may cross anil 
interlace. These tumors, (^spcH'ially the small-ct^lled forms, are, as a 
rule, denser and lirnuM- and less mahgnant than other forms of sar- 
coma, but to this there* iwo many i^xiH^ptious. They may be tMicap- 
sulatinl or iniiltrating. To this class In^long the growths formerly 



24:4 



TUMORS. 



described as fibro-plastic tumors and recurrent fibroids. They fre- 
quently occur in the periosteum, subcutaneous tissue and muscle : 
in the uterus, and in various glands, notably in the mamma, tes- 
ticle, thyroid, etc. These forms are among the most frequent of the 
sarcomata. 










Fig. 109. -Smat.t, Round-celled Sarcoma of Liver. 

Round-celled Sarcoma. — Of these there are two classes — 1, small 
round-celled sarcomata, and, 2, large round-celled sarcomata. 

1. The small round-celled sarcomata consist of cells of about the 
size and appearance of lymph cells (Fig. 109), and may have much 







"^liit 



Fig. 110.— Large Round-celled Sarcoma of Leg. 



or little intercellular substance, which may be irregularly disposed or 
arranged in large meshes resembling alveoli. In many cases, so small 
is the quantity of intercellular substance that it is difficult of detec- 
tion without special modes of preparation. These tumors are apt to 
contain many blood vessels, and be A^ery soft and succulent. Their 
growth is sometimes rapid and they are often ver^- malignant. 



TUMORS. 



•Z4:0 



They most frequently occur in the connective tissue of the mus- 
cles and fasciae, in bone, and in lymph nodes {lijiapho-sarcoma). 
They also occur in the internal organs, not infrequently in the brain, 
associated with glioma as glio-sarcoma. 

2. In the large round-celled sarcomata (Fig. 1 1 o) the cells vary in 
size, but are usually very much larger than in the last variety. Their 
nuclei are usually large iind contain prominent nucleoli. They, too. 
are often very vascular, and contain a variable quantity oi basement 
substance. They are occasionally alveolar in character. They are, 
as a rule, less soft and malignant than the small-celled varieties. 

The round-celled sarcomata were formerly supposed, on account 
of their macroscopical and clinical resemblance to some of the soft 
forms of carcinoma, to belong to these tumors, and were called me- 
dullary cancers. 




K\*/?--kV4;- / ;# *vS?-*-,'- ■ 'lift'/ 







Fig. 111.— Melano Sarcoma from Submaxillary Eegion. 



Melano-Sarcoma. — These tumors consist most frequently of spin- 
dle cells of various sizes, although cells of other shapes frequently 
occur in them. They are characterized by the presence in the cells, 
and less fretpiently in the intercellular substance, of larger ami 
smaller particles of brown or black pigment (Fig. 111). The pigment 
is usually quite irregularly distributed in patches or streaks, and is 
located chiefly in the cell body. They arise most frequently in the 
skin and in the choroid. Pigmented moles of the skin often form 
tlieir starting points. They belong to the most malignant of tumors. 
Tliey very readily form metastatic tunicn-s in various ])arts of the 
body, wliich are, like the parent tumor, pigmented. 

Various forms of tumors may contain brownish ])igment deposited 
in them by the degeneration of the luemogUUnn from extra vas^ited 
blood; these should not be mistaken for nu»huu>tio sarcomata. 

Myeloid or (ti(nif-c('//('(l Stn-conia. — Tun\ors of this class ari^ 
usually formed chietiy of spheroidal or fusiform cells of variable size. 



24:(5 



TUMORS. 



but their characteristic feature is the presence of larger and smaller 
multinuclear cells, called giant cells (see foot note on page 171). 
These are closely intermingled with the other cells, and may be very 
abundant or very few in number (Fig. 112). Giant cells may occa- 
sionally occur in other tumors, but are most abundant and charac- 
teristic in these. These tumors are chiefly formed in connection with 
bone, and may commence in the marrow or in the periosteum. They 
are sometimes very soft and vascular, and subject to interstitial 
hemorrhages. Some of these vascular sarcomata were formerly 
classed together with other kinds of vascular tumors as fungus haema- 
todes. Some of the forms of epulis are giant-celled sarcomata. 







Fig. 112.— GiAiJT celled Sarcoma of Bone. 



When these tumors originate in the marrow of the long bones, 
which is a favorite place for them, they are apt to cause resorption 
of the bone ; and although the tumor may be for a long time enclosed 
b}" a shell of new-formed bone, which enlarges with the enlarging 
tumor, it usually, sooner or later, breaks through this and infiltrates 
adjacent tissues. They are liable to form metastases and frequently 
grow to a very great size. The periosteal forms are apt to be firmer 
in texture, and are prone to the development of irregular masses of 
new bone ^vithin them, thus forming one of the varieties of osteo- 
sarcoma. 

Osteo-Sarcoma. — These are spindle or round-celled tumors, usu- 
ally, but not always, connected with bone, in which irregular raasses 
of bone tissue are present. The bone is usually of irregular atypical 



TUMORS. 



;^4? 



structure, the re^^ular larnellation and typical Haversian canals 
being usua;lly absent. They may form metastases which present 
similar characters. 

Calcification, which should be distinguished from ossification, 
may occur in various forms of sarcoma. 

Anglo-Sarcoma. — In many of the sarcomata in A^arious parts of 
the body the blood vessels form so prominent and important a fea- 
ture as to give special character to the growth, not alone hj their 
size and general prominence, but sometimes by the peculiar arrange- 
ment which their presence gives to the cells. While in most of the 
sarcomata the blood vessels have a very important influence in deter- 
mining the topography of the tumor, in most of the denser and in 






^^. 
~^^< 

















Fig. 113.— Angiosarcoma of Liver. 
The thin-walled blood vessels, around which the tumor cells are formed, are irregularly dilated. 



many of the softer varieties this influence is not easily traced. In 
many forms, however, particularly those which are soft and very 
cellular, the cells are closely grouped around the vessels, as if the}' 
were developed in their adventiticB and had formed close sheaths 
around them. The masses of cells thus formed, with a bloixl vessi^l 
for a centre, may be closel}' packed together in long string.^ w\\\\ 
more or less frequent anastomoses (Fig. 11')), ov they may be ar- 
ranged in rounded grou{)s, giving to (he tumor an alveolar ap}HMr- 
ance. 

In other cases the blood vessels may appvVir a^ i-liaracteristi^' fac- 
tors simply on accoimt of tluMr size or n^lativi^ abundance. 

Sometimes the walls (^'i the blood vessels and tlu^ adjacent tissues. 



248 



TUMORS. 



in these as in other forms of tumors, undergo a pecuhar hyahn de- 
generation, giving to the whole or to parts of the tumor a more or 
less gelatinous appearance. Such tumors are not very common, and 
are frequently grouped in an ill-defined class called cylindroma. 

Alveolar Sarcoma. — Sometimes, as above stated, the basement 
substance of the sarcomata, particularly in some of the round-celled 
varieties, is quite abundant and arranged in a ^vide-meshed net, in 
.the meshes of which the cells lie. These spaces are called alveoli, 
and this variety of structure has acquired importance from the gene- 
ral resemblance which these tumors have to the well-defined and 
characteristic alveolar structure which many of the carcinomata ex- 
hibit. It is true that occasionally the resemblance is very close 
indeed, but usually the sarcomata present a more or less intimate 




Fig. 114.— Myxo-Sakcoma of Pharynx. 



relation between the cells and basement substance. The cells usually 
do not simply lie in the cavities, but are often attached to the inter- 
cellular substance, which not seldom sends finer trabeculae into the 
alveoli between the cells. Sometimes a careful shaking of sections 
in water is necessary to reveal the characters of the reticulum. The 
cells, moreover, are usually, though not always, distinctive in cha- 
racter. This form of tumor is, in some cases at least, determined, as 
above stated, by the new formation and peculiar arrangement of the 
blood vessels. Tumors of this kind are not common, but may occur 
in the skin, IjTnph nodes, bones, and pia mater. They are usually 
very malignant. 

Mixed Fotnns of Sarcoma. — In addition to the above more or 
less well-defined forms of sarcoma, there exist various modifications 



TUM(;KS. 



249 



which have received special names. The sarcomata in which cysts 
form, either by the softening of tissue hy degeneration, ov ])y the 
dilatation of gland ducts hy pressure, or by the new formation of 
tissue in gland ducts or alveoli which dilate w^ith the growth of the 
tumor, have received the name of cysto-sarcomata. 

Mucous degeneration is frequent in the various forms of sarcoma. 
A combination of myxoma and sarcoma — myxo-sarcoma — is com- 
mon (see Fig. 114). 

Combinations of sarcoma with fat tissue, Iqjo-sarcoma ; with 
glandular structuTes, adeno-sarcoma (Fig. llo) ; with cartilage, 
chondrosarcoma ; with muscle tissue, myosarcoma ; and with va- 
rious other tissues, are of frequent occurrence. Some forms oi pnam- 
raoma, or '' brain sand,""* found chiefly in the dura mater, are fibro- 






l7i 




Fig. 115.— Adeno-Sarcoma of Parotid. 



sarcomata which have undergone calcification, the lime being do- 
posited in lamellated masses of various shapes within them. 

Some of the soft papillomata and warts, and occasionally the 
polypi of the mucous membranes, belong to the type of sarcoma or 
mj^xo-sarcoma. 

The so-called chloromata, which have been found in a variety of 
places in the body, but are rare, are apparently forms of sarcoma. 
Chloroma is characterized by a greiMiisli color, tlu^ nature of which is 
not known. 

ENDOTHELTOAIA (ENDOTHEIJ.VL SAKC'OM.O. 

Under the name c//(/o///(7/(// sarcoma/it ov cudotJu'liomata are 
grouped a. number of tumors which on the one hand are closely re- 
lated to the sarcomata in genesis, and in some cases in appearance, 
24 



250 TUMORSc 

Avhile on the other hand some of them so closely resemble some forms 
of carcinoma as to be diflficult of distinction from them. The endothe- 
lioma ta originate in that form of connective-tissue cells called endo- 
thelium, and seem to develo^D by a proliferation of these. Sometimes 
the cells of the endotheliomata resemble closely the normal endothe- 
lium ; sometimes, however, they differ considerably from them, being 
occasionally very large, often thick and irregular in shape, and even 
nearly cylindrical or cuboidal. They are associated with a more or 
less abundant vascular stroma, which may be alveolar in formation. 
In this case, as in alveolar sarcoma, it may often be seen that the 
cells have an intimate relationship to the trabeculse of the stroma, and 
to the arrangement of the blood vessels the general topography of 
the tumor may be due. 

Developing from the endothelium of the lymph vessels, these tumors 










'■' ^ "^^ 



■%^\t>\^^-^ \^'fS-%a=^^- r%^ 












Fig. 116.— Endothelioma (Endothelial Sarcoma) of Dura Mater. 

sometimes exhibit a structure closely simulating that of tubular 
glands lined with more or less cuboidal epithelium. 

Sometimes the cells of the endotheliomata are packed together in 
dense concentric masses (Fig. 116), which may have a glistening ap- 
pearance, and such tumors are sometimes called cholesteatomata. 
Although, for the most part, the peculiar glistening appearance of 
these tumors is due to the closely packed thin cells which compose 
them, they not infrequently contain crystals of cholesterin, sometimes 
in large quantities, which raay share in producing their characteristic 
appearance. But the cholesterin may be absent, or present in small 
amount. 

The endotheliomata may occur of considerable size and be nodu- 
lar ; or they may be multiple, numerous small tumors being scat- 
tered over the surface of the part in which they grow ; they may 



TUMORS. 251 

even form a thicker or thinner peUicle over surfaces, or cause adhe- 
sions between adjacent organs. They may form metastases. They 
occur in the dura mater and pia mater, in the pleura and peritoneum, 
and have been described in the lymph nodes, ovary, liver, brain, tes- 
ticle, and glandula carotica. 

LIPOMA. 

Lipomata are tumors formed of fat tissue. The fat tissue occurs in 
lobules and is similar to normal fat, except that the cells and lobules 
are usually larger and less regularly arranged. There may be little 
connective tissue in the tumors, when they are very soft, almost fluc- 
tuating — lipoma molle — or there may be so much as to give the 
tumor considerable Rrmness—fibirj-Upoma. They may be in part 
transformed into mucous tissue — myxo-lipoma. Cartilage not infre- 
quently develops in them, or they may undergo partial calcification. 

Occasionally the blood vessels are very abundant and dilated — 
anqio-lipoma. They are usually sharply circumscribed, but may 
infiltrate surrounding tissues. They are not infrequently pedicu- 
lated. They sometimes grow to enormous size and may ulcerate. 

They are usually isolated, but may be multiple. They are the 
most common of tumors, occurring usually in the subcutaneous or 
other fat tissue. They may occur in the mucous membrane of the 
gastro-intestinal canal, in the peritoneum, more rarely in the dura 
mater, kidney, liver, and lungs. They are benign tumors, not form- 
ing metastases ; but they may be deleterious by ulceration or gan- 
grene, and when not fully removed may exhibit local recurrence. 

CHONDROMA. 

These tumors, composed of either of the physiological forms of 
cartilage, are usually hard, but sometimes quite soft. The cells do 
not present the same uniformity in size, shape, number, and relative 
position that they do in normal cartilage. Sometimes they are verv 
large, spheroidal, and grouped in masses, and again small and tar 
apart. They are frecpiently fusiform or branching. Fibrillar con- 
nective tissue in varying (juantity is usuall}' present in the chondro- 
mata, either as a capsule, or running in bands betwiHMi the nodules 
of cartilage, or passing in fascicles into them (Fig. 1 1 D. The carti- 
lage may change to mucous tissue, forming nifi.vo-vhomJroiua ' (Fig. 
118) ; the cells may undergo fatty degeneration or they may c\dcify 



' This change of one form of tissue into another is oalloil m(7(z;)/<i«i'<i (see j"kiige 
74), and is not imcomiuou among tumors formed on the eouuective-tissue tyj)e. 



252 



TUMORS. 



or ossify. Chondromata frequently form a part of mixed and com- 
plex tumors. 

They may form in connection with bone or cartilage, and are 
often traceable to irregularities in foetal development. Or they may 



■"■yi^O^te.. 









v%j\ ' -^ - y'--^'-'^':^^^-^^^^ 



'IM^ 



- ^'■-:m^■■■■-m:■^ 



»fi|p/s: 






^lllSiii^^l 



■ r\--'-:'^^ 




Fig. 117.— Chondroma of Subcutaneous Connective Tissue. 

occur in soft parts where cartilage is not normally present, as in the 
parotid, testicle, mamma, and ovaries, where they are apt to be 











^:^ 



C) 







Fig. 118.— Myxo-Chondroma of Cervical Region. 



mixed with other tissues ; or in subcutaneous connective tissue and 
fascise. 

They are in general benign tumors, but metastases sometimes oc- 
cur, most frequently in the lungs, sometimes in the heart. 

Small hyperplastic growths on the surfaces of cartilage are called 
ecchondroses. 



TUMORS. 253 



OSTEOMA. 



The formation of bone in the body in abnormal places occurs 
quite frequently and under a great variety of conditions. It is on 
this account not easy to define the term osteoma, and it is frequently 
difficult to determine whether or not a given mass of new-formed 
bone is an osteoma or not. Bone tissue often occurs in tumors of 
the connective-tissue group as a secondary or complicating struc- 
ture — osteo-fibroma, osteo-chondroma, osteosarcoma, etc. It may 
occur in muscles as a result of certain exercises, or as a result 
of a peculiar inflammatory process (see Lesions of the Muscles), or 
it may occur in connection with chronic inflammation in a variety 
of tissues. A circumscribed mass of abnormal bone, not of inflam- 
matory origin, may be called an osteoma. Small masses of new- 
formed bone of various shape, projecting from a bony surface and 
frequently of inflammatory origin, are usually called osteophytes. 
Bony tumors projecting from the surface of bones are frequently 
called exostoses. 

An osteoma may be loose in texture, consisting of bone tissue 
similar to cancellous tissue ; or it may be denser, resembling compact 
bone tissue ; or it may be very hard and dense like ivory, so-called 
ivory exostoses. The difference between these forms lies chiefly in 
the varying number and size of the vascular and medullary spaces 
which they contain. 

Osteomata may develop in connection with the bone or peri- 
osteum, which is most frequently the case, or, independently of bone, 
in soft parts. 

New -formed bone has been found in the soft parts of the body, in 
the brain substance, dura mater, and pia mater ; in the pleura, 
diaphragm, and pericardium ; in the skin, choroid, air passages, 
lungs, and penis, and in other places. To what extent some of these 
bone formations may have been due to inflammatory action it is 
not possible to say, and it is quite probable that the fuller knowl- 
edge of the future may show relationships between the development 
of certain tumors and some forms of chronic inflammation which ^ve 
do not now recomiize. 

The growth of the osteomata is, ;is a rule, slow. Tlu'v aro benign 
tumors, and are not infreiiuently multi])le. 

OnOXTOAlA. 

Tumors are sometimes fcn-nied from the pulp during the tlevelop- 
ment of the teetli. When these contain dentin they arc called 
odontomata. 



254 



TUMORS. 



GLI03IA. 

Th3 giiomata are developed in connection with the characteristic 
connective-tissue framework of nerve tissue, the neurogha, which in 
structure many, though usually not all, of its cells closely resemble. 
Small cells with inconspicuous bodies and numerous delicate branch- 
ing processes are most characteristic ; but in connection with these 







m^m 



Fig. 119.— Glioma of Brain. 



there is usually a greater or less number of small spheroidal cells 
with proportionallj' large nuclei (Fig. 119). It is usually necessary 
to shake sections in water or carefully tease fragments of the tumor 




Fig. 1-20.— Neuroglia or " Spider " Cells prom Glioma op Brain. 

Teased specimen. 

in order to see the characteristic neuroglia or so-called ''spider ^^ cells 
(Fig. 120). These tumors may contain very numerous and frequently 
dilated thin- walled blood vessels. They may be very soft or mode- 
rately hard ; and, especially when occurring in the substance of the 
brain, are frequently not sharply outlined against the adjacent nor- 
mal tissue. They usually occur singly, and are comparatively slow 
in growth. 



TUMORS. 



255 



They are very apt to be complicated with other tumor tissue, 
forming (jUo-myxoma, fjlto-.sarcojna, etc. Owing to the abun- 
dance of thin-walled blood vessels and the softness of the growth, 
they are liable to interstitial haemorrhages, and may then, when oc- 
curring in the brain, readily be mistaken for ordinary ap^jplectic 
clots. They are liable to fatty degeneration. They usually occur in 
the brain, spinal cord, and in the optic and other cerebral nerves. 
The so-called gliomata of the retina are usually small spheroidal - 
celled sarcomata. 

Pure gliomata are benign tumors, though in their most common 
combination with sarcoma they may be very malignant. Their usual 
situation, however, is such as to riiake them almost always signifi- 
cant, although technically they are benign tumors. ' 

MYOMA. 

Tumors composed of muscular tissue are of two kinds, following 
the two physiological types of muscle tissue, the non-striated and the 
striated. 



^S3 



-«3!^^ 



:?^?^^3- 



^r^^i^^;:*^;^^^ 






%^ 



^-v: 




r. ^^^ 



Fig. 121.— Myoma of Uterus— Leiomyoma. 



I. Leiomyoma, Myoma levicellulare. — The characteristic ele- 
ments of these tumors are fusiform, smooth muscle fibres, ^^'ith 
elongated or rod-shaped nuclei. These are packed closely together, 
frequently interlacing and running in various directions, and are in- 
termingled with a variable quantity of more or less vascular tibrillar 
connective tissue (Pig. 121). When, as is not infrequently the case, 
the connective-tissue elements are present in large amount, the tumor 
is called fibro-m yoma. It is' not always easy in sections to distinguisli 
between these tumors and certain cellular tibroniata. but the cha- 
racteristic shape of the isolated cells and tluMr nuclei, together with 

' Our knowle(Vii:c of the normal nouroiilia is still too meairre to ponnit us to multM-- 
stand voiy thoroui^hly this class of tumors, and to separate it as procisoly as oouKl Iw 
wished from certain of its allies among the abnormal connective-tissue growths. 



256 TUMORS. 

their uniformity in size, will usually suffice. These tumors are fre- 
quently infiltrated with lime salts, and, owing to their density and 
lack of blood vessels, they not infrequently degenerate, forming cysts 
or becoming gangrenous. They may occur singly or be multiple, 
are usually of slow growth, may be large or small, and are benign. 
They may occur wherever smooth muscle tissue exists. They are 
most frequently found in the uterus, where they are often multiple. 
They may occur in the wall of the gastro-intestinal canal, and have 
been seen in the bladder and in the skin of the nipple and scrotum. 
The so-called hypertrophies of the prostate, so frequent in advanced 
life, are sometimes considered leiomyomata of the interstitial muscle 
tissue of that gland. 

II. Myoma striocellulare, or Bhahdoinyoma. — In these rare tu- 
mors striated muscle fibres are the characteristic elements. They 
very rarely compose a great part of the tumor, but are intermingled 
with other elements, fibrillar connective tissue, spindle-shaped and 
spheroidal cells of various forms, which often appear to be incompletely 
developed muscle cells. They are not infrequently associated with sar- 
comatous tissue. Blood vessels and sometimes nerves are also present. 
The muscle fibres differ, as a rule, from normal striated muscle fibres 
in their arrangement, which is usually quite irregular, and also in 
size, being in general smaller than normal fibres, although var\^ng 
greatly. The sarcolemma is either absent or incompletely developed. 
These tumors are usually small or of moderate size, and are sui3posed 
to originate from inclusions of cells destined to form muscle tissue in 
places where they do not belong. 

In the heart and certain other muscular parts small circumscribed 
masses of striated muscle tissue have been described, and are some- 
times called Jiomologous rliahdoinyomata. But genuine heterolo- 
gous rhabdomyomata are, in almost all cases thus far recorded, 
confined to the genito-urinary organs, kidney, ovary, and testicles. 
The writer has described an exceptional case of rhabdomyoma occur- 
ring in the parotid gland. ^ 

These tumors, when not associated ^vith other and malignant 
tumors, are benign and are of much greater theoretical than practical 
interest. 

NEUROMA. 

A true neuroma is a tumor containing new-formed nerve tissue. 
Such tumors are comparatively rare. Tumors developed in the con- 
nective tissue of nerves and composed usually of fibrous or mucous 
tissue are common, and are frequently called neuromata, but they 
should be called fibromata or myomata, etc., of the nerves, or false 

^ American Journal of tlie Medical Sciences, April, 1883. 



TUMORS. 257 

neuromata. The true neuromata are of two kinds, ganglionic or 
cellular neuromata and fibrillar neuromata, depending upon the 
character of nerve tissue which they contain. The gangHonic neu- 
romata — neuroma ganglioniforme — in which new-formed nerve cells 
are present (Fig. 122), are found associated with other structures in 
certain of the teratomata in the ovaries, testicles, and in the sacral 
region ; they also occur in the gray matter "of the brain . They have 
been found in the suprarenal glands. 

The fibrillar neuromata are, according to Yirchow, of two kinds, 
myelinic and amijelinic, depending upon whether the nerve fibres 
which they contain are medullated or not. The neuroma rayelini- 
cum is the more common and the best understood. The medullated 
nerve fibres in these tumors are associated with fibrillar connective 
tissue, and are usually curled and intertwined in a most intricate 
manner. They occur either singly or multiple on the peripheral 




Fig. 12-^.— Neuroma ganglioniforme. 
From the suprarenal gland. 

nerves. They may occur m considerable numbers as nodular tumors 
on the branches of a single nerve trunk, or they may form an irregu- 
lar, diffuse, nodulated enlargement of the nerve branches — ple.viform 
neuroma. These neuromata may or may not be painful. The}' not 
infrequently form at the cut ends of the nerves in amputation stumps. 
They ai'o benign tumors, never for;ning metastases. 

The false neuromata (Fig. 12;]) are myxomata. or fibromata, m- 
sometimes myxo-sarcomata of the nerve sheaths or intrafascimdar 
connective tissue, and may occur singly or multiple. In tlio lattoi- 
case they may affect the branches of a single nerve trunk. c>r they 
may be found on nearly all the oerebro-spinal ptn*iplieral nerves. 
Tlie writer has described a, case (Fig. 124) in wliich over elevtMi 
hundred and eighty-two distinct tumors were found distributed 
over nearly all tlie peripheral utM-vi^s o^ iW^ btnly.' 

' Americfin Jonnml o'( (ho "Modionl Scioncos. .Tulv. 1880. 



258 



tu:mors. 



The nerve fibres in these tumors may be crowded apart by the 
new growth and considerably atrophied ; or, in cases in which the 




Fig. 123.— Fibroma (False Neuroma) op Lumbar Nerve. 

The fibrous tissue is loose in texture and in places cedematous, so that it considerably re- 
sembles mucous tissue. 

tumor is composed of soft tissue, as in myxoma or the soft fibro- 
ma, they may pass through or around the tumor entirely un- 
changed. The multiple false neuromata are in many cases con- 
genital. 




Fig. 124.— Multiple Fibromata (False Neuromata) of P>'eumogastric Nerve. One-quarter 
natural size. 



ANGIOMA. 



Angiomata are tumors consisting in large part or entirely of new- 
formed blood or lymph vessels or cavities. In many tumors of vari- 
ous kinds the new-formed or the old blood and lymph vessels may be 



TUMORS. 



250 



very abundant or prominent by reason of their dilatations ; the ves- 
sels of otherwise normal tissues may also be largely dilated, thus 
simulating vascular tumors. These are, however, not true angio- 
mata, although sometimes .reckoned among them, and in many cases 
closely allied to them. Such are the so-called arterial varix, or cir- 
soid aneurisms, and haemorrhoids, and various lymphectasise. True 
an^^omaf a are of two kinds — I., Hcemancjioma, and 11., Lymph- 
angioma. 

I. Hcemangiomata. — These tumors are of two types : 1. Those 
formed largely of capillary blood vessels with either thin or thickened 
walls, embedded in a more or less abundant connective-tissue stroma. 
These are called simple angiomata or angioina telangiectoides. The 
walls of the vessels in these tumors are frequently dilated or pouched. 




Fig. 125.— Angioma telangiectoides (Vascular Ntevus). 
From skin over scapula of child. 

and usually form a tangle of curled and intertwined vessels (Fig. l'2o). 
They occur most frequently in the skin or subcutaneous tissues, 
usually about the face, and may project above the general surface 
or be on a level with it. Such are the so-called rascidiO' na'ri, or 
straivhernj iHavhs, which are usually congenital. They are some- 
times sharply circumscribed, and sometimes merge imperceptibly 
hito the surrounding skin. They sometimes occur in tht* mucous 
membraiies, in the mamma., bones, and brain. Tliov are benign 
tumors, never forming metastases, but may be associated with sar- 
comata. 

'Z. The second form of luBmangioma, t'alled angioma varcrnosnniy 
consists largely of a series of intiM-communicating, irregular-shaped 
larger and smaller blood spaces lineil witli eudt>theHuin, and sur- 
rounded by a variable (piautity of librillar connective tissue, whirh 



260 



TUMORS. 



may contain smooth muscle cells (Fig. 126). They resemble the erec- 
tile tissue of the corpora cavernosa of the penis and clitoris. They 
are apparently formed by a dilatation of old and new-formed caj^il- 
laries and veins. They are sometimes erectile and sometimes pulsa^t- 
ing, and are not infrequently multiple. They may be seated in the 



^-^^?g-<^ 
















Fig. 126.— Angioma cavernosum of Liver. 



skin and subcutaneous tissue, forming the so-called projecting nsevi, 
or in internal organs. They are often found in the liver and less 
frequently in bone, the brain, spleen, uterus, kidney, intestines, blad- 






















i^r 



y&^ 



Fig. 127. — Congenital Lymphangioma prom Arm op Child. 

der, and muscles. They are usually of little significance, though 
they may give rise to haemorrhages. 

II. Lymphangioma. — These tumors consist of dilated lymph 
channels, which either preserve approximately the general shape of 
the original lymph vessels, or are distinctly cavernous in character, 
or even cystic (Fig. 127). They probably originate in part in new- 



<» 



TUMORS. 2i}\. 



formed, in part in old lymph channels. A strict distinction between 
tumors formed by a dilatation of preformed and new-formed lymjjli 
channels is not possible, owing to the very primitive character of some 
of the ultimate lymph spaces and our lack of knowledge of their exact 
relations to adjacent parts. 

In the lymphangiomata there may be much or little connective 
tissue between the dilated channels, which are usually filled with a 
translucent or milky fluid resembling, and probably identical with, 
the normal lymph. These tumors are usually congenital, but are 
sometimes acquired. They usually occur in the skin as soft, some- 
times considerably, sometimes but slightly elevated tumors, and may 
occur in the tongue — some forms of so-called macroglossia. They 
are benign tumors, but may rupture, giving rise to a serious lymph- 
orrhoea. 

TUMORS IN WHICH EPITHELIAL CELLS ARE PREDOMINANT OR 
CHARACTERISTIC ELEMENTS— EPITHELIAL TUMORS. 

I. Adenoma. 

II. Carcinoma. 

General Considerations. — The tumors thus far described in de- 
tail, with the exception of the gliomata, are formed on the type of 
tissues which develop from the parablast. The epithelial tumors, on 
the other hand, originate in one or other of the layers of the archi- 
blast, and we have accordingly two series of criteria by which to de- 
scribe and identify them : first, morphological, and second, histoge- 
netic criteria. 

While in the main, in the normal body, the general distinctions 
between epithelial and other, tissues are fairly well marked, there are 
still particular cases, especially those in which epithelial tissues are in 
process of physiological growth or rejuvenation, in which the dis- 
tinctions are quite ill-defined. When we remember the rapid growth 
of many tumors, the tendency to incomplete formation of their cells, 
their diverse seats, and the various complicating conditions under 
which they originate and develop, it does not seem strange that the 
exact limitations of this class of tumors are not easy to fix, nor that 
they seem sometimes to merge into one another and into tumor tis- 
sues belonging to other classes. If epithelial cells, inider all circum- 
stances, had a definite and characteristic structure, or if, on the other 
hand, we could alwavs know whether a e:iven coll Lircnip oriirinated 
in epithelium or not, the matter of distinguishing between tumors of 
this and other classes would be simple and easy enough. As it is, in 
some cases both morphological and histogenetic criteria fail us, and 
the clinical history and gross appearance are not characteristic. Sucii 
cases — which are indeed rare, but which do sometimes occur — suL^i^est 



262 TUMORS. 

to us the possibility that the desirabihty of accurate classification has 
led us into seeking distinctions which Nature herself has not sharply 
drawn. While these difficulties in special cases must be acknowl- 
edged, the distinctions are in the main definite enough, and very use- 
ful both for clinical and scientific purposes. 

Epithelial tumors always contain, in addition to the more or less 
characteristic cellular elements, a connective-tissue stroma which 
gives them support and carries the vessels. This stroma may be 
sparse or abundant, may contain few or many cells, is sometimes ar- 
ranged in irregular fascicles or bands, and very frequently forms the 
walls of well-defined, variously-shaped spaces or cavities called alve- 
oli, in which the epithelial cells lie. The epithelial cells, in most 
cases, lie along the walls of the alveoli without an intimate connec- 
tion with them, as is the case in the alveolar sarcomata. They are, 
moreover, packed together without more intercellular substance than 
the usual cementing material common to epithelial cell masses. 'In 
this lack of fibrillar intercellular substance within the alveoli, and in 
the loose relationship between the cells and the alveolar walls, lie in 
many cases the chief morphological distinctions between certain car- 
cinomata and alveolar sarcomata. 

In certain of the epithelial tumors there is a reproduction of typi- 
cal gland tissue of various kinds, depending upon the seat and condi- 
tions of growth of the tumor. Such tumors are called adenomata. 
A simple hypertrophy of a gland, or an increase in its size by exces- 
sive growth of its interstitial tissue, does not constitute an adenoma. 
There must be an actual new formation of more or less typical gland 
tissue. This is not always or frequently of exactly the same charac- 
ter as the gland tissue in which it originates, and alvv^ays exhibits a 
certain lack of conformity to the type in structure and mode of 
growth. The alveoli and ducts usually have a lumen and some- 
times a membrana propria, but the cells may differ in shape from one 
another and from those of the gland from which they spring. 

Epithelial tumors in which there is no close conformity to a glan- 
dular type, but a lawless growth of various kinds of more or less 
typical epithelial cells in the meshes of an old or new-formed connec- 
tive-tissue stroma, are called carcinomata. 

It will readily be seen that there must be a border region between 
the adenomata and carcinomata, where conformity to the glandular 
type merges into the lawlessness of growth characteristic of carcino- 
mata. In this border region a certain degree of individual bias must 
be permitted in assigning a name to the new growth. In some cases 
a sharp distinction cannot be made, or the tumor may share in the 
characteristics of both, and then we very properly make use of the 
term adeno-carcinoma or carcino-adenoma. 



TUMORS. 



203 



I. ADENOMA. 

The structure of the ceUular elements of these tumors, and their 
arrangement into acini and ducts, vary even more than do those of 
the normal glands whose types they follow. The acini usually pos- 
sess a more or less well-defined lumen and membrana propria (see 
Fig. 128). The adenomata sometimes merge into the surrounding 
tissue, or are continuous with the gland tissue in which they ori- 
ginate ; sometimes they are distinct in outline and encapsulated. 
The interstitial tissue is sometimes abundant, sometimes sparse, and 
may contain few or many cells. The irregularities of their growth 




Fia. 1'28.— Adenoma of Mamma. 



often lead to the stoppage of the lumina of their ducts and the forma- 
tion of cysts. They may undergo mucous motamor]ihosis and mav 
become sarcomatous. 

Adenomata occur in the mamma, ovary, hvcr, kidney, thvroid. 
salivary, and lachrymal glands, and in the caruncle ; in the nuu'ou> 
membrane of the nose, pharynx, stomach, intestine, and uterus ; and 
occasionally in the sebaceous and sweat glands o( the skin. The so- 
called multilocular cystomata of th(^ (n'ary are among the most im- 
portant of the adenomata. There .ire nnmennis papillary and ]>oh-- 
l)oid growths, in gland ducts and on nuieons membranes, in wliii'h 
there is an actual new formation of gland epitlu^liuni; Init this is usu- 
ally secondary to a })rimary growth, beneath tht^ epithelial layer, o^l 



264 



TUMORS. 



some other tissue, such as fibrous or mucous tissue, and the new 
growth of gland epithehum simply keeps pace with the growth of the 













Fig. 1^9.— Adenoma op Stomach, 
A f orra which is on the border line of carcinoma. 



latter, to which it serves as an investment. Such growths are some- 




FiG. 130 —Adenoma op Antrum. 
This complex form of adenoma, somewhat resembling types of adenoma occurring in the 
ovary, is sometimes called cylindroma. 

times classed among the adenomata, but do not, strictly speaking, 
belong there. 



TUMORS. 265 

The adenomata are in general benign tumors, being slow of 
growth and locaHzed, but there are very important exceptions. 
Some of the adenomata of the stomach and intestines belong to the 
most malignant of tumors in rapidity of local extension, in the for- 
mation of metastases, and the development of cachexia. Certain of 
the adenomata of the mamma and thyroid are also very malignant. 
It should be remarked, however, that, as a rule, the malignant adeno- 
mata are those which, in structure, lie close upon the border line 
between tumors of this class and carcinomata (see Fig. 129), and by 
such observers as incline to lay more stress upon clinical than mor- 
phological distinctions they are usually classed among the latter. 

Adenomata are not infrequently of such bizarre types that their 
nature is not evident without very thorough study (see Fig. 130). 
Some of the atypical forms lie very close to the border zone of the 
carcinomata. * 

II. CARCINOMA. 

The tumors of this highly important class are composed, as above 
stated, of a connective-tissue stroma, forming more or less well- 
defined communicating spaces or alveoli, in which lie variously 
shaped epithelial cells arranged in an atypical manner. The stroma, 
containing few or many cells, may be, especially in the advancing 
portions of the tumor, composed largely of the old connective tissue 
of the part. It may, however, be entirely new formed. The cells 
which lie in the spaces or alveoli bear sometimes a very close, some- 
times but a very general resemblance to epithelium. 

It was formerly believed that new epithelium might be formed, 
both from old epithelial cells and from the connective-tissue ceUs, 
and possibly from white blood cells, and among many observers this 
belief still exists and has never been disproved. Still, ^\nthin the last 
twenty years the opinion that new epithelial cells in tumors arise 
exclusively from old epithelium has found general acceptance, and 
for very good reasons. N"o one has actually seen an epitheHal cell 
originate under the microscope, and until this can be done our beliefs 
must rest upon indirect observations. In the first place, all the epi- 
thelial structures in the embryo originate in the archiblastic layei-s, 
that is, in those layers which are largely characterized by the pre- 
sence of epithelium (see page 232). In regeneration after an injury 
in the adult, a study of the successive phases of the process shows 
that new epithelium is always forminl in continuity with the old. and 
apparently by a proliferation of old epitheHal cells. Epithelial tu- 
mors are almost exclusively found iu parts normally containing epi- 
thelium, and frequently tlie new growth can be distinctly seen to be 
continuous with the old cells. 



266 TUM.ORS. 

Finally, the observations on mitosis have greatly strengthened the 
view that new epithehal cells in tnmors are always derived from 
the old. 

The occurrence of primary epithehal tumors in parts of the body 
in which epithehmn does not normahy occur, as in bone and the 
lymph nodes, has been recorded; but these may have been metasta- 
tic tumors, in which the primary tumor was small and overlooked, 
or .they may have been displaced embryonic germs, which, according 
to Co b ri helm's hypothesis (see page 528), would explain their hetero- 
logous occurrence. These possibihties of error should be taken into 
the accotmt in the apparently exceptional cases, and it is to be re- 
marked that these are becoming less and less as our knowledge m- 
creases and our technical f acihties for research improve. 

A considerable number of the tumors formerly described as 
heterologous primary carcinomata are now known to be formed by 
proliferation of endothehiun, and hence to belong to another class — 
endothehoma — although sometimes considerably resembling the car- 
cinomata in structure. 

The occurrence of primary carcinoma of the peritoneum, pleura, 
and pericardium, which is not infrequent, was for a long time inex- 
phcable, and seemed whoUy inconsistent with the behef that all car- 
cinomata originate in epithehal ceUs. Because it was, and to a large 
extent still is, beheved that the fiat cells lining these great body cav- 
ities are true endothehujn, and closely related in origin, as they are 
■ in structure, to the genuine endothehum of the blood and lymph ves- 
sels, etc. 

But recent embryological researches have shown that this behef 
is not AveU founded. It was formerly thought that the great serous 
cavities were large lymph vessels formed by the sphtting apart of 
the connective-tissue layers of the mesoblast. But we now know 
that the great primitive body cavity, which after a time becomes di- 
vided into the pleural, pericardial, and peritoneal sacs, is originally 
an outgrowth from the alimentary canal. The epithehmn of the ali- 
mentary canal, however, is of archiblastic origin, while the connec- 
tive tissue, blood and lymph vessels are developed later from the 
parablast. Geneticahy, therefore, the so-called endothehal cells lin- 
mg the pleural, pericardial, and peritoneal cavities are of archiblastic 
origin and belong among the epithehmn. Thus a fuller knowledge 
of the histogenesis of the cells lining the great body cavities has 
shoTvn us that the occurrence of primary carcinoma in these cavities 
is not only not in contradiction with the principle of the epithehal 
origin of carcinoma, but stroDgiy confirmatory of it. 

A great practical difficulty in the descrij^tion, and, to beginners. 
in the recognition, of the carcinomata and their varieties, hes in the 



TUMORS. 



207 



great diversity in shape which their cells present. It should he 
always borne in mind that the shape of cells depends in part upon 
their inherited tendencies in growth, which we cannot see under 
the microscope; but to a greater degree uj)on the varying conditions 
of nutriment and pressure to which they are exposed during Hfe. 
In the normal body these conditions conform to a certain standard, 
so that cells of a given kind at a given stage of development are 
cipproximately similar. 

In tumors, however, the lawlessness and lack of fixed conditions 
in growth are such that we may have many young and SitjiAcsil so- 




FiG. 131.— Cancer Cells infiltrating the Tissue in the Vicinity op a Tcmor. 

From carcinoma mammoe. 

called indifferent forms of cells ; while even the adult forms may 
depart widely from normal shapes. Thus, in cylindrical-celled carci- 
nomata there are many fully developed cells which are never cy- 
lindrical ; there are many others not fully developed which are quitv^ 
indifferent in form, looking just like many other yoimg cells — cells 
which are not, but which are destined to become, epithelium. 
Finally, we have the cells produced by ordinary intlammatory pro- 
cesses about and witliui tlie tumor, whicli acts hke an irritatiui;- 
foreign body. Thus it is that tliere is no morphologically charac- 
teristic '^ cancer cell," as was formerly supposed. Some of them are 
typical and some not, and the more tyj)ical ones may look just like 



2G8 



TUMORS. 



normal epitlielial cells, and the atypical ones just like simple inflam- 
matory cells, or young connective-tissue cells, or white blood cells. 
It is always in the topography, together with the general characters 













</ .^ 






£^ 



V.' 



it 









A 















Fig. 132.— Metastatic Carcinoma in Lymph Vessels op the Pleura, 
(Tlie primary tumor was in the liver.) 

of the cells and the situation of the growth, that Ave must seek for the 
evidences of the nature of a given tumor. 

The carcinomata are verj- prone to local extension, the advancing 




Fig. 133.— Inflammation in Carcinoma Uteri. 
Showing acciimulation of pus cells between the epithelial cells of the tumor, 

tumor cells in the periphery making their way through the IjTnph 
spaces and forming new foci (Fig, 131). Metastasis is of frequent 
occurrence in some forms, and takes place chiefly, though not ex- 
clusively, through the lymph vessels, frequently involving adjacent 



TUMORS. 2f'/.) 

or remote lymph nodes. The growth of the tumor cells in the l3^mph 
vessels, either in the immediate vicinity of the original tumor or fol- 
lowing metastasis in a distant part of the body, may cause these to 
become distended, and, on free surfaces like the pleura and peri- 
toneum, to form a whitish, elevated network. Transverse sections of 
such distended lymph vessels are shown in Fig. 132. The secondary 
tumors are in the main similar in general structure to the primary 
foci, but may differ from them in vascularity and the abundance of 
the stroma, or in the shape of the cells. The carcinomata are, as a 
rule, malignant tumors, but the different forms vary much in this 
respect. They are liable to fatty, colloid, mucous, and amyloid de- 
generation, and are especially prone to ulceration, to haemorrhage, 
and simple inflammation (Fig. 133). They may become partially cal- 
cified, and are not infrequently combined with other forms of tissue 
in the mixed tumors. 

They are more frequent in middle and old age than in the young, 
but they may occur at any age. 

Forms of Carcinoma. — In certain cases of carcinoma which 
occur in the skin and in some mucous membranes, the cells present 
the structure and general characters of the epithelium of the part in 
which they occur ; and since here the tendency of the cells as they 
approach the surface is to become flattened or squamous, these tumors 
are called Squamous or Flat-celled Carcinomata, or simply Epithe- 
liomata. 

In another class of tumors, such as frequently occur in the gastro- 
intestinal canal and uterus, the cells are more or less cylindrical in 
shape, forming a palisade-like lining to the irregular alveoli : such 
tumors are called Cylindrical-celled Carcinomata, although here 
again many of the cells are not cylindrical at all, but may have a 
great variety of forms. 

There is a third and very common form of tumor, in which the 
epithelial cells have no constant characteristic shape, but vary as 
much as do the cell forms in the various glands of the body. Such 
tumors are conveniently classed together as Gland-celled Carcinoma, 
or Carcinoma simplex. 

In addition to these forms there are several others which depend 
for their characteristics upon various metamorphoses or degenery- 
tions, or upon the preponderance of one or other of the anatc^nioal 
constituents of the growth. It will be most convenient to give a brief 
description of these various kinds, one after another, with the under- 
standing that they are not absolute specitic forms, but are simply 
varieties which it is convenient to recognize for c'linical as wt^ll as 
anatomical purposes. 

Flat-celled Carcinoma, or Kpiflwlioma, — These tumors occur iu 



270 TUMORS. 

the skin and in the mucous membranes which are covered with 
squamous epithehum. The cells present all of the various forms 
w^hich normally exist in these parts — the cuboidal and polyhedral cells 
of the rete Malpighii, as well as the more superficial flattened forms 
(Fig. 134). Frequently the spined cells, or so-called "prickle cells," 
are largely reproduced. Ha\dng to a certain extent the same life 
history as the cells in which they originate, many of the tumor cells 
become dry, thin, and horny, like the epidermis cells, as they grow 
older ; and since their growth and changes often occur within the old 
lymph spaces of the affected tissue or in the new-formed alveoli, the 












#7" 






s -.^^ ^^;&;v?> ' ' 



■^, ..'A.i ''Tr --M^r 



. A /'( ^1*, 










Fig. 134.— Epithelioma op the Neck. 
Shows epithelial pearls, spined. cells, and reticular masses of variously shaped epithelial cells. 

cells are sometimes packed together in spheroidal, concentric masses 
called " epithelial pearls," which may sometimes be seen with the 
naked eye upon or near the surface of the growth (Fig. 135). The 
new cell masses may be large or small, may be separated by much 
or little stroma ; often form reticular masses, and may infiltrate the 
tissues deeply or remain near the surface ; or may project above the 
surface, forming wart-like or papillary growths. These tumors fre- 
quently ulcerate on the surface, and the skin about them is apt to 
become thickened (see Fig. 136). 

They are most apt to occur in the skin, especially in those parts in 
which it becomes continuous ^vith mucous membranes — lips, exter- 



TUMORS. 



271 



nal nasal openings, eyelids, labia, and glans penis — and are frequent 
in the mouth, oesophagus, vagina, and about the cervix uteri. 

There are also carcinomata of the skin, composed of cuboidal cells 






^' 














Fig, 135.— Epithelioma of Axillary Lymph Node. 
This metastatic tumor was secondary to a large epithelioma of the back of the hand, Fig. 
136. The small cells with darker nuclei are the cells of the lymph node. It shows the epilheliai 
pearls. 

arranged in tubules or masses, which do not follow the type of the 




'\ 



\ 






Fio. 13(5.— Epithelioma of Back of Hand. 
The flat tumor occupied uearlj- the entire back ot" thi^ hand, and was uloeratiui:: at the contrtv 
The fijjfure shows the edge of the tumor and a portion of the uIcim*. The papilhv of the skin over 
thtu^lgo of the growth are hyportropliied, and the tissue about intiUratovl with small spheroidal 
cells. Fig. 1,').') sliow.s asiH"(it>n Iroiu a nu^tastntic mnior of tlio axillary lymph node in this case. 

epithelium of the skin, but rather that of tho swoat glands or soba- 



272 



TUMORS. 



.<r' 




-^C*s. 




/:vwwr;»iriifc^-i;-^=-;rs»i>isiU>Si^^i--xUi:'C;;i^ 






Fig. 137.— a Small EpiXHSLioiiA of the Side of the Nose. 















/!^'3 






if 



^•?^r^ ' 



'j -^ 



fc- 



re 



^>--p/^<^.~-^ 






x^ 



4«/ 












^fe 






"/ -/ ^ 6^ 






:^ '«'./; 



- ^>A'';?vy:- 



FiG. 138.— Epithelioma of Nose. 
A portion of the tumor shown in Fig. 137 more highly magnified. 



j^ 



\Q^ 



TUMORS. 



27:3 



ceous glands. These tumors are found most frequently on the nose 
and eyehds (Figs. 137 and 138). 

Sometimes certain of the cells in an epithelioma appear to coal- 
esce, forming a large multinuclear mass. This variety of epitheli- 
oma is sometimes called giant-celled epithelioma. 

Flexner ' has described a rare tumor arising from the epithelial 
layers of the retina, which he calls a neuro-epithelioma. 

Epitheliomata are apt to recur if not thoroughly removed, and 
may form metastases, but in general they are the least malignant of 
the carcinomata. The prognosis is in most cases good if there is 
early and complete removal. 

Cylindrical-celled Carcinoma. — These tumors, closelv allied to 








Fig. 139.— Carcinoma Mamm^ (Scirrhus variety). 



some forms of adenoma (see Fig. 120), occur in the stomach, intes- 
tines, and uterus. The cells may be only in part cylindrical, the re- 
mainder having various shapes, and all being loosely or closely packed 
in larger or smaller alveoli. They may have much or little stroma. 
They merge imperceptibly into the next class : 

Gland-celled Carcinoma, or Carcinoma simplex. — These, which 
are by far the most frecpient of the carcinomata of internal parts, are 
characterized by the alveolar structure ami by the absence of any 
special characteristic shape in the cells, which may be spheroidal, 
polyhedral, fusiform, or cuboidal. They may ov may not i*esemble the 

' Flexner, "A Peculiar Glioma (nearoepithelioma) of the Kctina." Johns Hopkins 
Hospital Bulletin, August, 181)1. 



274: TUMORS. 

epitheliiun of the gland in which they originate. Ther are usually 
nodular tumors, and mav be hard or soft. If the stroma is abundant 
and dense, and preponderates over the cellular elements, the tumor is 
usually hard and is called scirrlius ov fibro-carcinoma (Fig. 139). 
If, on the other hand, the cellular elements largely preponderate, the 
tumor is usuallv soft, and, if it do not contain too manv blood ves- 
sels, may have a general resemblance to brain tissue, and is then 
called encephaloid or inedidlary cancer j or, better. Carcinoma 
molle (Fig. 140). These are among the most malignant of the ear- 
cinomata. 





Jii'' v./ t?l' t ''' ! ' l&'i' -'•''- '^f ^' 




^Vi*-.-1-\f - " > ■ ■«. J:,^ :-■ r . . .31, 




Fig. 140.— ^Iedut.t.ary Caects-oma of tee Stomach (Carcinoma mojle). 

The intercellular tissue in these carcinomata may become so abun- 
dant as to nearly obliterate the cellular elements, but it is doubtful 
if they ever undergo spontaneous cure in this way. These tumors 
may be hard in one portion and soft la another. They may contain 
very many blood vessels, C. telangiectoides. They occur as primary 
tumors in the mamma, hver, thyroid, sahvary, and prostate glands, 
in the pancreas, kidney, testicle, and ovary. 

Colloid Carcinoma. — The cells of certain carcinomata, esf)ecially 
of the gastro-intestinal canal, may suffer a more or less complete mfil- 
tration with a translucent material somewhat resembling gelatin and 
called colloid, whose nature is not well understood. Sometimes this 



TUMOKS. 






infiltration is only partial, when the protoplasm of the cells may be 
more or less encroached upon by the translucent droplets of the col- 
loid material ; but in other cases, over large areas the cells are par- 







Fig. 141.— Colloid Carcinoma op Ehctum. 

tially or entirely destroyed, and replaced by the new material, so that 
the alveoli of the tumor are distended by it, and their walls appear 







v^> 






Fig. 14*3.— Carcinoma myxomatodks Mamm.«- 



very distinct in the midst of the colloid substance (Fig. 1 1 0. In sucli 
cases the alveolar structure of the tunun* is sometimes vorv evident 
to the naked eve, and these tumors are therefore often called (//r(V)/(fr 



27Q TUMORS. 

carcinoma. Sometimes only a part of the tumor is affected in this 
way. 

Carcinoma my xomat odes. — The celkilar elements of carcinomata 
may suffer mucous softening, and thus larger and smaller cysts 
containing a mucous fluid are sometimes formed. To this form 
of metamorphosed tumor the above name is sometimes apphed, but 
it more properly belongs to carcinomata in which the stroma is com- 
posed of mucous tissue (Fig. 142). Such tumors are most frequently 
found in the gastro-intestinal canal and mamma. 

2Ielano- Carcinoma. — Tumors of this class are rare, and are cha- 
racterized by the presence of a variable quantity of black or brown 
pigment jDarticles either in the stroma or in the cells. They are 
usually soft and malignant, and most f requentlj^ occur in the skin. ^ 

'^Bibliography. — The most extensire and important work on tumors, containing 
a vast store of information, is that of Rudolph Virchoic, '' Die krankhafte Ge- 
sch-wlilste." It is not completed and is somewhat old, but is still invaluable as a work 
of reference. The section on tumors in Yon Pitha and Billroth's work on surgery 
(" Handbuch der allgemeinen u. speciellen Chirurgie "), which comprises the first sec 
tion of the second volume, by I)}\ Lilcke, is very complete. A valuable bibliography 
and digest of recent observations on tumors will be found in the last edition of BircJr 
Hirschfeld' s work on pathological anatomy (" Lehrbuch der pathologischen Ana- 
tomic "), vol, i. ; also in Zieglefs " Lehrbuch der path. Anat.,'* Band i., 7th ed., 1892. 
An important resume on the Malignant Tumors in Childhood, by Stern, maybe found 
in the Deutsche med, Wochenschrift, June 2d, 1892, p. 494. 



PART III. 



MOEBID AISTATOMT OF THE OEGAXS. 



THE I^EP.VOUS SYSTEM. 



THE MEMBEANES OF THE BRAIN. 

THE DURA MATER. 

The dura mater is a dense connective-tissue membrane which 
serves the double purpose of a periosteum for the inner surface of 
the cranial bones, and of an investing membrane for the brain. It 
is itself but poorly supplied with blood vessels, but it contains the 
large venous sinuses which carry the blood from the brain. Lesions 
of the dura mater, therefore, are apt to be associated with lesions of 
the cranial bones, of the pia mater, or of the venous sinuses. 

In young children the dura mater adheres closely to the inner 
surface of the cranial bones, in adults it is more readily detached, 
and in old persons it is again more adherent. Chronic inflammation 
of the external layers of the dura mater also renders it more adherent 
to the bones. 

HEMORRHAGES. 

We find extravasations of blood between the dura mater and 
the cranial bones, in the substance of the membrane, and between the 
dura mater and the pia mater. 

The haemorrhages in the substance of the dura mater are usually 
small and of little consequence. 

The haemorrhages between the dura mater and the pia mater tx^- 
cur with chronic pachymeningitis, or are derived fvom the vessels of 
the pia mater. 

The lijiemorrhages between the dura mater and the cranial bones 
are produced by blows and injuries of the head. They are often of 
considerable size, separate the membrane from the bones, and may 
compress the brain. They are often associated with lacoratii>u of 
the brain, and luDuiorrliages between the dura mater and pia mater. 

The pressure on the head of the infant in labor may proiluce, in 
addition to the extravasations of blood betu'een the bi>nes and the 
pericranium, additional extravasation between the bones and the 
dura mater. 



280 THE NERVOUS SYSTEM. 

THROMBOSIS. 

Thrombosis of the venous sinuses is not uncommon. Any in- 
flammation of the dura mater is liable to produce it ; injuries and in- 
flammations of the brain and pia mater, of the cranial bones, of the 
middle ear, and of the scalp may also produce thrombosis. The 
changes in the blood produced by the exhausting 8.nd infectious dis- 
eases may induce thrombosis of the venous sinuses, as they do of 
the veins in other parts of the body. There are also rare cases in 
which such a thrombosis is developed without discoverable cause in 
persons pre^dously healthy, and produces marked symptoms and 
death. 

Some of these thrombi are firm, of white or red color, and ap- 
parently produce no secondary lesions. 

Others are of firm consistence, but they produce softening with 
small haemorrhages of portions of the brain. In these cases the 
thrombus extends from the venous sinus into one of its veins, and 
the portion of brain belonging to this vein is softened and haemor- 
rhagic. Such a softening of the brain is often attended with in- 
flammation of the pia mater. 

In other cases the thrombi are soft and purif orm ; fragments of 
them become detached and lodge as infectious emboli in the arteries 
in different parts of the body. 

INFLAMMATION. 

Inflammation of the dura mater is cdl\(^A pachymeningitis, and 
this may involve the external layers of the membrane, jDachy menin- 
gitis externa, or the internal layers, pachymeningitis interna. It 
may furthermore be either acute or chronic. The tissues of the sub- 
stance of the dura mater participate to a greater or less degree in 
these changes, but the chief lesions are upon the surfaces. 

Acute pachymeningitis externa is usually secondary to injuries 
or diseases of the cranial bones ; thus fractures of the skull, either 
■depressed or not, ostitis, caries, suppurative inflammation of the in- 
ternal and middle ear and mastoid cells, may produce it. The dura 
mater is usually congested, thickened, and softened, and may present 
small ecchymoses. The inflammation is usually suppurative, and 
23US may accumulate between the membrane and the bone, or in the 
substance of the membrane. The areas of inflammation are not usu- 
ally extensive. It sometimes induces thrombosis of the venous sin- 
uses, and sometimes gangrene of the dura mater occurs. The inflam- 
mation may extend to the inner surface of the dura mater, to the pia 
mater and brain, or it may remain localized and undergo resolution. 

Acute pachymeningitis interna may be secondary to inflamma 



THE NERVOUS SYSTEM. 281 

tion of the external surface, or it may occur as a complication in 
pyaemia, puerperal fever, chronic diffuse nephritis, in the exanthe- 
mata and erysipelas, or idiopathically. There is a general or cir- 
cumscribed production of fibrin and pus, so that the internal surface 
of the membrane is lined with a layer of soft, yellow exudation. 

Simple chronic pachymeningitis consists in the formation of new 
connective tissue in the dura mater, by which it becomes thicker 
and in many cases abnormally adherent to the bones of the skull. 
This thickening may be general or circumscribed, and may involve 
the entire thickness of the membrane. Not infrequently, when the 
external layers are especially involved, firm adhesions to the skull 
occur, with ossification of the outer layers, so that shreds of the 
membrane containing little masses of bone (osteophytes) remain 
sticking to the skull when the membrane is stripped off. 

There is an important form of chronic inflammation of the inter- 
nal layer of the dura mater, called pachymeningitis interna hcEinor- 
rhagica, characterized by the formation of layers of new delicate 
connective tissue with numerous very thin-walled blood vessels from 
which the blood is prone to escape. The membrane may at first ap- 
pear as a delicate fibrinous pellicle, with small red spots scattered 
through it, or it may look like a simple reddish or brown staining of 
the inner surface of the dura mater. Microscopical examination 
shows this membrane to consist of numerous blood vessels, mostly 
capillaries with very thin walls, which may be distended or pouched, 
and which have grow^n out from the vessels of the dura mater (Fig. 
143). Between the vessels is a homogeneous or slightly differentiated 
basement substance, containing a variable number of spheroidal, 
fusiform, or branching cells. Red blood cells in variable quantity, 
and blood pigment in various forms, frequently enclosed in the new 
cells, and small calcareous concretions (brain sand) (Fig. 144), also 
lie in the intervascular spaces. In more advanced stages the new 
membrane may become greatly thickened, its outermost layers being 
changed into dense fibrous tissue with obliteration of the vessels ; 
while the more recently formed layers are similar in structure to 
those at first developed. Considerable blood usually escapes from 
the vessels of the new membrane by diapedesis, in all stages of its 
formation, and the vessels are also very liable to rupture, giving rise 
to extensive hiiemorrhages either into the substance of the membrane 
or between it and the pia mater. Sometimes masses of new tissue 
and blood, from half an inch to an inch or more in thickness, are in 
this way formed, greatly compressing the brain. These new mem- 
branes are most freiiuently fcn-med ovor the convexity of the brain, 
but may extend over nearly thi> entire surface of tlie dura matiM'. 
Sometimes, when old, the entire niembranc, ilensely ]>igmented and 
26 



282 



THE NERVOUS SYSTEM. 



firm, lies loosely beneath the dura mater without compressing the 
brain or giving any chnical indication of its presence. The mem- 
brane may induce chronic changes in the pia mater, with or ^vithout 
accompanying changes in the cortical portion of the brain. 




Fig. 143— Chronic Pachymeningitis interna hemorrhagica. 

Rarely, serum accumulates between the layers of the new mem- 
brane, and in this way cysts of large size may be formed. In rare 
cases diffuse suppuration of the entire new membrane occurs. 




Fig. 144.— Brain Sand from Pachymeningitis interna. 



The slighter degrees of this form of inflammation may occasion 
no symptoms during hf e. They are not infrequently found in per- 
sons suffering froin various chronic brain lesions and from chronic 
alcoholism, but they may occur unassociated with complicating lesions. 



THE NERVOUS SYSTEM. 283 

The more advanced forms of the lesion are frequently found in idiots, 
epileptics, etc. 

Tubercular pachymeningitis may occur secondarily to that form 
of inflammation in the pia mater or the bones, or as a part of general 
miliary tuberculosis. The tubercles may be situated on either sur- 
face of the membrane or in its substance, and may be single or aggre- 
gated, forming large masses. 

Syphilitic pachij meningitis manifests itself by the formation of 
;so-called gummy tumors upon either the external or internal surface 
of the dura mater. These tumors may be single or multiple, and 
vary greatly in size. They may be accompanied by simple inflam- 
matory changes in the dura mater in their vicinity. They may 
undergo suppuration with the formation of abscess ; the inflammation 
may extend to the pia mater, inducing simple or syphilitic meningi- 
tis and adhesions between the dura mater and pia mater. The gum- 
mata may, on the other hand, when occurring on the outer surface 
of the membrane, cause absorption and perforation of the bones of 
the skull. 

TUMORS. 

The most common tumors of the dura mater are sarcomata, and 
of these the spindle-celled forms are of more, the round- and polyhe- 
dral-celled of less frequent occurrence. They may grow from either 
surface of the membrane. Some of the round- and polyhedral-celled 
forms are soft and very vascular, and are apt to involve the neigh- 
boring pia mater and brain tissue, or the bones of the skull, which 
they may perforate. They sometimes project through the opening 
in the skull in fungous, bleeding masses. 

Psammomata are small globular tumors, often multiple and 
pediculated, growing from the inner surface of the dura mater. 
They are usually composed of tissue sarcomatous in character, and 
contain variously shaped calcareous concretions similar in appearance 
to the so-called brain sand. ' 

Endotheliomata. ^ — These tumors may grow inward or outward, 
causing pressure on the brain or absorption and perforation of the 
bones ; they often attain considerable size. Some of those tumors 
somewhat resemble certain forms of epitheliomata (see Fiu'. 1 1'')\ and 
have often been described as primary carcinomata. 

Fibromata and Lipomata occur rarely in thi* dura mater and 
are of small size. 



' For a study of psammoma consult EniM, " \JqWv Psmmm^nia.** In Ziosjlor'sBei- 
trilg-e zur path. Auatoniie, Bd. xi., page 2;U. 18!)'2. 

'F'or a consideration of tumors of the dnvix niator allied to the endotheliomata con- 
;sult Dogond, Arch, de jNIed, Kxji.. ]May tst, 1890. 



284 THE XERYOUS SYSTEM. 

Small Chondromafa are sometimes fomid comiected with the 
dura m.ater at the base of the brain. 

Osteomata. — In addition to the formation of osteophytes in 
chronic external pachYmeningitis, plates and, more rarely, globular 
masses of bone may be formed in the dura mater, unconnected ^th 
the bones of the skull. They are most frequently found in the falx 
cerebri, but may occur elsewhere. The new bone may be dense or 
loose in texture, and usually produces no symptoms. 

THE PIA MATER. 

The external surface of the brain is iuA^ested by a connectiYe-tis- 
sue membrane which coYers the conYolutions, dips down into the 
sulci, and extends into the Yentricles. This membrane is abundantly 
supplied with blood Yessels, and from it numerous Yessels extend into 
the brain, so that any disturbance in the circulation of the blood in 
the pia mater iuYolYes a disturbance in the circulation of the blood 
in the brain also. 

The connectiYe tissue which makes up the pia mater is arranged 
in a series of membranes and fibres reinforced by elastic tissue, so ar- 
ranged as to form a spongy membrane containing numerous ca^^ties 
more or less fihed YT-th fluid. These caAuties are continuous Y-ith the 
periYascular spaces which surround the Yessels that pass from the pia 
mater into the brain. 

The outer layers of the pia mater are the most compact, and are 
coYered on their outer surface by a continuous layer of endothehal 
ceUs. This external layer of the pia mater is often described as a 
separate membrane caUed the '*' arachnoid,'" but it is reaUy only part 
of the pia. 

The deeper layers of the pia contain the blood Yessels. The mem- 
branes and fibres which compose the pia mater are partly coated Y^th 
ceUs which haYe irregular and dehcate cell bodies and large, dis- 
tinct nuclei. 

In aU inflammations of the pia mater the inflammatory products 
regularly collect in the spaces Yrithin it. 

Along the borders of the longitudinal fissure, and, more rarely, 
on the under surface of the brain, are a number of small, Y^hite, firm, 
irregular bodies — the Pacchionian bodies. They Yary in their size, 
their number, and in the extent of the surface of the hemispheres 
which they coYcr. They may perforate the dura mater, or, more 
rarely, the waU of the longitudinal sinus, and may produce erosions 
of the skull bones. They are composed of fibrous tissue and may un- 
dergo fatty or calcareous degeneration. As they are so commonly 
found and are not knoYm to be of any pathological significance, they 



THE NERVOUS SYSTEM. 285 

may almost be regarded as normal structures ; at any rate, we do 
not know what causes them or their variations in size and number. 

The pia mater is frequently thickened, opaque, and white, either 
in diffuse patches or, more commonly, along the course of the ves- 
sels. In other cases single or multiple small white spots, of the size 
of a pin's head or smaller, may be seen in the membrane, not appre- 
ciably elevated above the surface, but due to localized thickening. 
These slight opacities of the pia mater are commonly believed to be 
dependent upon repeated congestions of the membrane or upon 
chronic meningitis, but there is no evidence that this is always the 
case. They are most frequently found in old persons, but may exist 
at any age, and do not necessarily indicate the pre-existence of dis- 
ease, although similar appearances are common in the chronic insane 
and in drunkards. 

The amount of blood contained in the vessels of the pia mater af- 
ter death varies greatly, and is by no means a reliable indication of 
the amount present during life. In general anaemia the vessels of 
the pia mater may contain little blood, but, on the other hand, they 
sometimes seem to contain a relatively larger amount than other 
parts of the body. In oedema of the brain and pia mater the vessels 
of the latter may contain but a small amount of blood. 

CEDEMA. 

The quantity of serum beneath the pia mater and infiltrating 
its tissue is very variable in amount. It may accumulate as a 
result of atrophy of the brain substance or of venous hyper^emia, 
and sometimes is, and sometimes is not, accompanied by oedema of 
the brain substance. It may be diffuse or localized. It is not infre- 
quent to find in hospital patients suffering from chronic nephritis, 
cardiac or pulmonary disease, or chronic alcoholism, a very consid- 
erable amount of serum in this situation, and 3'et the patient has 
been free from cerebral symptoms. In other cases, again, tliis same 
serous effusion affords the only explanatii^n of grave cerebral symp- 
toms. It is necessar}" to be very careful in judging of the import- 
ance of this accumulation of fiuid. 

It should always be borne in mind that an accumulation of fiuid 
beneath and in the meshes of the pia mater mav occur as a result of 
post-mortem changes. 

HYPER.EMIA AND HAEMORRHAGE. 

The pia mater may be h f/pcrtviiiic in early stages i^f meninuitis. 
after death from dehrium treinens or following ej^ileptic convul- 
sions, from various infectious diseases, certain jioisons. the pn^sentv 



286 THE XERTOUS SYSTEM. 

of tunlors or exiiaations pressing on the veins, as well as from gen- 
eral and local diseases of the circulatory ajiparatiis. But whether 
they are overfilled or comparatively empty after death seems to de- 
pend upon the position in which the body has lain, upon the time 
Trhich has elapsed between death and the examination, upon the 
rapidity with which the blood coagulates, and upon conditions en- 
tirely imknown to us. 

Hcpmorrliage. — This may occur either into the space between the 
dura mater and the pia mater — intermeningea.J hcemorrhage — or in 
the meshes of the pia or between the latter and the brain. It may 
be due to injury, to ruptru'e of aneurisms or otherwise diseased blood 
vessels, to thromboses of the venous sinuses, or to causes vrhich ^we are 
unable to ascertain. Haemorrhages, without known cause, not infre- 
quently occur in the substance of the pia mater in young children, 
but in adults they are apt to be the result of injury. Multiple ecchy- 
moses, however, in the substance of the pia mater sometimes occur 
in infectious diseases and also in acute inflammation of the pia mater. 
Hsemorrhao'es in the brain substance mav lead to the accmnulation of 
blood beneath or in the meshes of the pia mater. IntermeningeaL 
haemorrhage in infants as a result of injiuy during birth is not un- 
common. Small, and sometimes considerable, extravasations of blood 
may occur from diapedesis, and sometimes, as a result of chronic 
congestion, degenerated blood pig-ment collects along the walls of 
the vessels. The extravasated blood in menino-eal haemorrhage, if 
small in quantity, may be largely absorbed, lea^dng a greater or 
smaller accumulation of pigment at the seat of the haemorrhage, and 
such pigmentations may last for a long time. 

IXFLAM3IATI0X. 

Inflammation of the pia mater is called lepto-meningitis. or sim- 
ply meningitis. AVe distinguish acute, chrome, tuberctdar, and syph- 
ihtic meninoitis. 

Acute Jleningitis occurs most frequently as the characteristic 
lesion of epidemic cerebro-spinal meningitis : it is a not very infre- 
quent comjDhcation of pneumonia, Bright's disease, typhus and ty- 
phoid fever, and the exanthemata ; it is secondary to injuries and 
inflammation of the cranial bones, of the dura mater, and of the 
middle ear, and it is sometimes an idiopathic lesion. 

In any case of acute meningitis the inflammation is apt to extend 
downward and involve the pia mater of the cord. It may also in- 
volve the ependyma of the ventricles, and cause the distention of these 
cavities with seriun. This latter condition belongs especially to 
voting children. 



THE NERVOUS SYSTEM. 



287 



There are two anatomical varieties of acute meningitis, which 
give, however, the same cKnical symptoms, 

(1) Acute cellular meningitis'. — The pia mater is somewhat con- 
gested, its surface is dry and lustreless, and it is somewhat opaque. 
These changes in the gross appearance of the membrane are not 
marked and are easily overlooked, but the minute changes are more 
decided. There is an abundant production of cells somewhat re- 
sembling the cells which coat the surfaces of the membranes and 
fibres which make up the pia mater (Fig. 145). This cell growth is 




^-.-^,. >*i ..-- ^^^^-"&^/<M^^-^:^ 



->S>-t^~^«v>tt; 








1^ ;^: V-:; :^J§r^.)^^^^^ 



general, involving the pia mater over most of the surface of the brain. 
The inflannnation, then, is one which results in the prcxluction, not of 
fibrin, serum, or pus, but of new connective-tissue cells. This form 
of meningitis is of frequent occurrence and is attended with the ordi- 
nary clinical symptoms of acute meningitis. 

(2) Acute exudative meningitis is characterized by the accu- 
mulation, chiefiy in the meshes of the pia mater and along the walls 
of the blood vessels, of variable quantities of serum, fibrin, and pus. 
Sometimes one, sometimes another of these exudations prejnuub^ 
rates, giving rise to serous, fibrinous, or purulent forms of the iu- 
fiammation. The absolute quantitii^s, too, of tlie exudations vary 



288 



THE NERVOUS SYSTEM. 



greatly. In some cases death may be caused Tvatli so slight a for- 
mation of exudation that to the naked eye the pia mater may look 
quite normal or perhaps only moderately hypersemic or oedematous ; 
the microscope, however, in these cases, will reveal pus cells in 
small numbers, and sometimes flakes of fibrin in the meshes and 
along the walls of the vessels. In other cases turbid serum in the 
meshes of the membrane is all that can be seen, and the microscope 
shows the turbidity to be due to pus cells or a small amount of fibrin. 
Again, either with or without marked oedema of the pia mater, yel- 
lowish stripes are seen along the sides of the veins, sometimes ap- 
pearing like faint turbid streaks, and at others dense, opaque, thick, 
and wide, and almost concealing the vessels. These are due to the 
accumulation of pus cells and fibrin in large quantities along the ves- 















^.■,:.;/f,:i^>:i 






Fig. 146.— Acute Exudative Meningitis. 

a, convolutions of cerebrum ; 6, pia mater thickly infiltrated with pus ; c, blood vessels entering 
brain from pia and surrounded by a zone of pus cells ; d, congested blood vessels of pia mater ; e^ 
smaller blood vessels of pia, around which pus cells are collected in dense masses. 

sel, and they are best seen and most abundant around the larger veins 
which run along over the sulci. In still other cases the infiltration 
with pus and fibrin is so dense and thick and general that the brain 
tissue, convolutions, and most of the vessels of the pia mater them- 
selves are concealed by it. This is usually of a greenish-yellow 
color, and is sometimes so thick as to form a sort of cast of the brain 
surface at the seat of the lesion (Fig. 146). Sometimes extra vasated 
red blood cells are mingled \vith the other exudations, as the result of 
diapedesis. Microscopical examination shows numerous white blood 
cells sticking in the walls of the veins and capillaries, or the vessels 
may be blocked vdth them. It is evident that a large part of the 
pus cells accumulate as the result of emigration. The connective- 
tissue cells of the pia mater may be detached from their places or 



THE NERVOUS SYSTEM. 



289 



■degenerated. In some cases there are considerable accumulations of 
pus between the pia mater and the brain substance and along the 
vessels which enter the latter. More rarely pus is found upon the 
free surface of the membrane. The brain substance may be com- 
pressed by the accumulated exudation, so that the convolutions are 
flattened. The cortical portion of the brain may be simply infiltrated 
with serum — oedematous — or it may undergo degenerative changes, 
or it may be the seat of punctate haemorrhages. Not infrequently 
the inflammation extends to the ventricles, which may contain puru- 
lent serum, and to the pia mater of the cord. This form of inflam- 
mation is most frequent on the convexity of the brain, but may ex- 




FiG. 147.— Fatty Degeneration of Cells along the Blood Vessels of the Pia !Mater 
AFTER Exudative Meningitis. 

From the pia mater of a child five years old. 

tend, or even be confined to the base. It may be localized, but 
frequently extends widely over the surfaces of the hemispheres. 
Bacteria are often present in the exudation. For their relationship 
to the lesions see Cerebro-spinal Meningitis. 

When recovery from acute exudative meningitis occurs there 
may be fatty degeneration of the cells which have accumulated in 
the pia mater, particularl}^ along the vessels (Fig. 147), and this may 
produce white patches in the membrane and threads along the blood 
vessels, which resemble the appearance of an accumulation of exuda- 
tion in the acute stage. Fatty degenerativ>n of the blood vessels aiul 
cells of the pia mater may also occur wiihout at'ute intlanunatory 
changes. 



290 



THE NERVOUS SYSTEM. 



Sometimes, in children and young adults, inflammatory clianges 
in the ventricles persist for days and weeks after the subsidence of 
the inflammation of the pia mater. 

ChroRic Jleningitis. — Either the pia mater at the base of the 
brain alone may be inflamed (basilar meningitis), or the pia mater 
over the convexity alone, or the entire pia mater, or circumscribed 
patches of the membrane. The pia mater is thickened and opaque, 
the thickening being sometimes very considerable. There is a forma- 
tion of new connective tissue and a production of pus, fibrin, and. 




Fig. 14S.— a 3Iilt^ry Tubercle of the Pia ]Mateb, x 850 and reduced. 
Composed of a simple aggregation of cells. 



serum : the relative quantity of these inflammatory products varies 
in different cases. Firm and sometimes extensive adhesions may be 
formed between the dura mater and the pia mater. N"ot infrequently 
the cortical portions of the brain participate in the morbid process, 
and we find an infiltration of small spheroidal cells around the blood 
vessels, thicken nig of the walls of the vessels, and degenerative 
changes and atrophy of the nerve tissue. Xew connective tissue may 
also form in the brain substance, v^hich may become closely adherent 
to the pia mater. The ventricles of the brain also may contain an 
increased amount of serum and may be dilated, and the ependyma 



THE NERVOUS SYSTEM. 



20 r 



may be thickened and roughened. This form of inflammation may- 
be the result of injury or disease of the cranial bones, or secondary 
to chronic pachymeningitis or to inflammation of the brain substance. 
It may occur in the vicinity of tumors of the brain or meninges. It 
may be a complication of chronic diffuse nephritis or the result of 




Fig. 149.— Miliary Tubercle of the Pia Mater of a Child, undergoing Cheesy Degenera 
TioN AT ITS Centre. 

chronic alcoholic poisoning. It may occur in marked form in the 
general paralysis of the insane. 

Tubercular Meningitis. — This is especially characterized by the 
formation in the pia mater of miliary tubercles, associated with more 
or less well-marked exudative inflammation. It may occur in adults 
and in children, but is more common in the latter. The dura mater 
may be unchanged, or its inner surface may be sprinkled with mili- 




^^^J.^iP i'^-:-f '^if^f^I^T^ 











■ s 




^^iMi^^*^^5,«^SfciV"u«*J 



iiai' 



Fig. 150.— a Miliary Tubercle of the Pia Mater. 
Situated on the wall of a small artory which is the seat of endarteritis. 

ary tubercles. The pia mater may or may not be congested ; it may 
look dry on the surface or it may be unhMuatous. UsuaUy the brain 
seems to All the cerebral cavity to an unusual degree, and the convo- 
lutions are flattened. If the i)ia mater be onhMuatous tlie serum 
maybe clear, or turbid with pus and flbriu. The nieiubrane may ]>iv- 
sent any of the general appearances oi exudative meningitis. But 
always in addition to these, and sometimes without them, miliary 



292 THE NERVOUS SYSTEM. 

tubercles, either widely scattered or in great numbers, may be seen, 
usually more abundant over the sulci than elsewhere. They are 
usually more abundant at the base of the brain than on the con- 
Texity, and are frequently confined to the base. Some of the tuber- 
cles are so small as to be scarcely visible or entirely invisible to the 
naked eye ; others are as large as a pin^s head or larger. They are 
usually most abundant along the blood vessels, but may occur else- 
where. They may be formed in the membranous prolongations of 
the pia mater which dip into the sulci, around the vessels which enter 
the brain substance, in the choroid plexus and ependyma of the ven- 
tricles, and may exist in the spinal cord. 

The miliary tubercles do not all have the same structure. Some 
of them are simply small aggregations of round cells within the peri- 
vascular sheaths of the smaller arteries. Others are composed of 
small masses of polyhedral and round cells (Fig. 148) without any 



,v^^ *"^^ar r*i^rV ,^i^r;-_-. 
















Fig. 151.— Miliary Tubercles of the Epenbyma of the Lateral Ventricle, x 70 and reduced. 

basement substance between them, and without any special relation 
to the blood vessels. Many others have the ordinary structure of 
tubercle tissue, basement substance, polyhedral cells, and giant cells 
(Fig. 149). These tubercles are usually situated around or near a 
blood vessel, and this blood vessel is apt to be at the same time the 
seat of an obliterating endarteritis (Fig. 150). This form of tubercle 
is also prone to cheesy degeneration (Fig. 149). 

In children the ventricles are usually more or less distended by 
an accumulation of transparent or turbid serum, and the walls of the 
ventricles may be studded with miliary tubercles (see Figs. 151 and 
152). In adults the ventricles are less frequently involved. The 
brain tissue around the ventricles is often softened. The central 
canal of the spinal cord may also be dilated. It is the dilatation of the 
ventricles which causes the flattening of the convolutions, and the 
flattening is usually in direct proportion to the amount of accumulated 



THE NERVOUS SYSTEM. 



203 



fluid. Miliary tubercles in the choroid of the eye are present in a 
considerable proportion of cases. 

The cortex of the brain may be hypersemic, and punctate haemor- 
rhages may be present in the cortex and in the pia mater. 

In almost all cases of tubercular meningitis there is tubercular 
inflammation in other parts of the body. 

In adults, as in children, while the tubercular inflammation is al- 

C©)f ^ ^ 







-ii .ktiJ--,l5 Jii; .^. i.' ,_i4it..'w»ji'jUiiW»i" 



Fig. 152.— a Miliary Tubercle of the Epkndyma of the Lateral Ventricle, uiagnified, 
X 500 and reduced. 

waj^s present, the accompanying simple inflammation may bo very 
slight or extensive, and the degree to "which it develops does not 
seem to depend upon the abundauce of the miliary tubercles. Cow- 
ing to the fretpiency of the dilatation of the ventricles with serum in 
children, the disease is often called acnlc Jiffdrocephalus. 

In both children and adults the tubercular intlaiumation may 
produce large masses (^f tubercular tissue, which undergo cheesy de- 
generation, in the pia. mater and tlie brain tissue. 



394 THE NERVOUS SYSTEM. 

Syphilitic Meningitis. — In this form of inflammation, which is 
usually circumscribed, there is a development of gummy tumors of 
variable size, frequently associated "with simple inflammation of the 
: membrane, either with the formation of serum, fibrin, and pus, or 
■with the development of new connective tissue and the consequent 
thickening of the membrane. The gummata may form in the pia 
mater covering the convexity, or at the base of the brain. They may 
grow outward, involving the dura mater ; or inward, encroaching 
upon or in vohdng the brain tissue. Although usually circumscribed, 
the syphilitic inflammation may occur as a diffuse thickening of the 
membrane. The syphilitic nodules, including the gummata and new- 
formed connective tissue, are often very small, but may be as large as 
a hen's Qg^. 

TUMORS. 

Hcematoyna. — In the cases of chronic pachymeningitis of long 
standing the new connective tissue may form large, flat cysts be- 
tween the dura mater and the pia mater, which may compress the 
surface of the brain. The blood originally contained in these cysts 
.may be absorbed and replaced by serum, the attachments to the dura 
mater may disappear, and the whole appearance becomes that of an 
independent cyst between the dura mater and pia mater. 

It is beheved by some observers that these cysts are not formed in 
this way, but that they represent a blood clot which has become en- 
veloped in connective tissue. 

Endothelioma. — We include under this name a considerable 
number of tumors which originate in the pia mater, the choroid plex- 
uses, and the ependyma of the ventricles. These tumors may reach 
a considerable size and compress the brain. For the most part only 
- a single tumor exists, but sometimes there are several, and in one 
case I (Delafield) found a large number of such tumors grooving 
from the dura mater and pia mater of the brain and of the spinal 
cord, and also from the choroid plexus. These tumors do not aU 
have the same structure. 

Some of them are composed of a connective-tissue stroma which 
• encloses regular spaces filled ■\vith large, flat, nucleated cells. The 
Avhole appearance resembles that of an ordinary carcinoma, but the 
cells are apparently of endothelial and not of epithelial origin. 

Some of them are composed of a connective-tissue stroma which 
forms cavities hned with cylindrical epithelium. In such tumors the 
stroma may grow so as to form papillae covered with cylindrical epithe- 
lium ; or in addition there may be mucous degeneration of the stroma. 

In some of them there is a connective-tissue stroma which con- 
tains large numbers of blood vessels. Around these blood vessels 
are arranged regular masses of polygonal cells — ^^angio-sarcoma.^^ 



THE NERVOUS SYSTEM. 295 

In some of them the stroma is scanty. The cells are numerous, 
large, flat, and arranged in little globular masses or nests. 

If in these little nests there is a deposition of the salts of lime, 
forming concretions like the so-called " brain sand,'^ the tumor is 
called a ^'psammoma.^^ 

Some of the tumors seem to be formed of very thin, nucleated 
membranes arranged in concentric layers like the layers of an onion. 

Some of the tumors are composed of balls or nests of large, flat, 
epidermic-looking cells, with which are found crystals of choles- 
terin — '^ cholesteatoma. '' 

Sarcoma. — Tumors belonging to the ordinary types of round- and 
fusiform-celled sarcoma, of myxo-sarcoma, and of myxoma are 
occasionally found in the pia mater. 

Fibromata, lipomata, chondromata, and osteomata are of rare 
occurrence. 

Cysts. — Small cysts are often found in the choroid j^lexus. Rare- 
ly such cysts reach a larger size, even as large as a pigeon's egg. 

Cysts of the pia mater containing serum, with walls and septa of 
connective tissue, and compressing the brain, have been described. 

Variously shaped pigment cells not infrequently occur in the pia 
mater, either scattered or sometimes in considerable masses : thev 
seem to have little pathological significance. JSTot infrequently thin 
plates of new-formed bone are found in the pia mater, associated 
with a thickening of the membrane. 

PARASITES. 

Cysticercus has been observed in the pia mater. 

THE VENTRICLES OF THE BRAIN. 
THE EPENDYMA AND CHOROID PLEXUS. 

As the lymph spaces of the pia mater and the ventricles of the 
brain are in communication, it might be supposed that they would 
share alike in the accumulation of fluids. This, however, is not the 
case. The membranes of the brain may be highly o?demc'itous while 
the ventricles contain about the normal quantity of fluid : o\\ on the 
other hand, the ventricles may be widely dilated and the i>ia mater 
unusually dry. Many of these varying ci^nditions may be umler- 
stood b}^ rcMuembering that the skull and spinal canal form a closed 
cavity, and that accumulations of fluid in one part must be at the 
expense of stnno material occui)ying other }>arts, either bU>od, serum, 
or brain tissue. It is not always easy to see. however, exaetiv how 
•the compensation (.)ecurs. 



296 THE NERVOUS SYSTEM. 

There may be an unusual amount of fluid in the ventricles of the 
brain as a result of post-mortem change ; in connection with senile 
or other atrophy of the brain, or in the general vascular changes 
which lead to oedema of the brain ; in connection "svith inflammation 
of the meninges or of the ependyma ; or under conditions which we 
do not understand, as in some cases of congenital and acquired hy- 
drocephalus. Accumulations of fluid in the ventricles are often 
called internal hyclroceplialiis to distinguish them from accumula- 
tions in the meninges — external hydrocephalus. 

INFLAMMATION". 

Acute Inflammation of the Ependyma {Acute Ependymitis). — 
In this condition, which may occur by itself, but is usually associ- 
ated mth inflammation of other parts of the brain, the ependyma is 
congested, the vessels are more prominent than usual and are often 
tortuous. The ependyma and the adjacent brain tissue may be 
thickened and infiltrated 'with pus cells, and the surface of the 
ependyma covered with fibrin and pus in variable quantity. The 
cavities of the ventricles may contain purulent serum. Small haemor- 
rhages may also be present in the tissue of the ependyma. This, as 
well as other forms of infiammation, is more common in the lateral 
ventricles than in the others, but not infrequently involves the fourth 
ventricle. The choroid plexus may participate in the inflammatory 
changes of the ependyma. Tubercular inflammation of the epen- 
dyraa is, as above mentioned, a not infrequent accompaniment of 
tubercular meningitis. 

Chronic Inflammation of the Ependyma {Chronic Ependy- 
mitis). — This lesion, which is much more common than simple acute 
inflammation of the ependyma, occurs under a variety of conditions, 
and its nature and causation are in general very obscure. The 
epend}Tna is thicker, whiter, and more opaque than normal, so that 
the vessels may be nearly or quite invisible. The thickening may 
occur in patches or diffusely, and the surface of the ependyma may 
be smooth, or roughened and granular. On microscopical examina- 
tion the surface of the ependyma may be covered with the usual 
epithelium, but the new connective tissue which forms beneath it 
often raises it up in places, causing the roughness of the surface. 
The new tissue is usually rather loose in texture and may contain 
many small spheroidal cells ; but it may be dense in texture and 
contain few cells. The brain tissue beneath the thickened epen- 
dyma may be softened or infiltrated mth cells. The sides of the 
ventricles may be grown together in places by the adhesion of the 
thickened and roughened ependyma. The ventricles usually con- 
tain more serum than normal, and sometimes this accumulation is so 



THE NERVOUS SYSTEM. 



297 



great as to cause an enormous dilatation of them. While these are 
in general the prominent lesions in chronic inflammation of the 
ependyma, the cases vary greatly in the degree to which these 
changes are developed. 

The accumulation of fluid and the«. dilatation of the ventricles 
being the most marked feature in all this class of lesions, they are 
often called chronic hydrocepJialus, and indeed in many cases we 
have no evidence that the change in the ependyma is an important 
or even an actual primary factor. 

We may, for convenience of study, consider three classes of cases 
of chronic hydrocephalus : first, congenital hydrocephalus in young 
children ; second, secondary hydrocephalus in children and adults ; 
third, primary hydrocephalus in adults. 




Fig. 153.— CoNGENiTAii Hydrocephalus in Child. About half natural size . 
a, a, dilated lateral ventricles; b, comua, unequally dilated ; c. third ventricJe; d, middle com- 



missure. 



1. Congenital Hydrocephalus. — The lesion may be in an ad- 
vanced stage at the time of birth, or it may be scarcely evident or but 
moderately developed. It may progress rapidly and cause the early 
death of the child, or it may develop gradually or come to a stand- 
still. In the more marked forms of the disease the ventricles are 
widely dik>ted and filled with serum, Avhicli is usually transparent. 
Not only the lateral ventricles, but also the third and fifth, may be 
involved ; the fourth is less apt to participate in the lesion, although 
it is sometimes dilated, as well as the central canal of the cord. 

The distention, especially of the lateral ventricles, may be so great 

that the brain tissue over the vertex is crowded up into a thin hivor 

biMiea,th tlie dura mater, or it may be entirely destroy ihI. When the 

dikitation of the vcMitricles is considerabU\ the convolutions are fiat- 

27 



298 THE NERVOUS SYSTEM. 

tened (see Fig. 153) and may be almost entirely obliterated. The 
skull bones may be thin and bulging over the forehead and vertex ; 
the fontanelles and sutures widely open. The ependyma in these 
cases is usually thick and rough, but it may be softened, and the 
blood vessels may be dilated. The basal portions of the brain may 
be flattened, but are usually much less affected than the upper por- 
tions. The brain tissue is usually soft and anaemic. 

2. Secondary Hydrocephalus. — This may occur in children and 
adults, and may be a result of epidemic cerebro-spinal meningitis, or 
of acute meningitis, or of chronic meningitis. It sometimes occurs 
in chronic alcoholic poisoning and in general paralysis of the insane. 
The amount of dilatation of the ventricles varies greatly in these 
cases, but it is never so great as in congenital hydrocephalus, and is 
not accompanied by the changes in the shape of the skull which 
form so prominent a feature in the latter disease, since the bones are 
firmer and the sutures united. In this form of chronic hydrocepha- 
lus the changes in the ependyma above described are usually more or 
less well marked, and they may be associated with the production of 
fibrin and pus. 

3. Primary Hydrocephalus in Adults. — The conditions leading 
to this form of lesion are not understood. It is apt to occur in persons 
over thirty years of age. Sometimes one, sometimes both lateral 
ventricles are dilated. The dilatation is usually moderate, sometimes 
very slight, and never as great as in congenital hydrocephalus. The 
ventricles usually contain transparent serum, and the ependyma is 
thickened and roughened. In some cases it is the only lesion found 
to account for the death of the patient. 



TUMORS. 

The new formation of connective tissue in the ependyma, al- 
though usually diffuse, may be circumscribed and form small, pro- 
jecting connective-tissue nodules, which may be reckoned among 
the fibromata. Small fibromata are sometimes detached from the 
walls of the ventricles and lie free in the cavity. Small liponiata, 
angiomata, and also sarcomata and gliomata occur rarely. Chon- 
dromata and angiomata may occur in the choroid plexus, and the 
latter are sometimes as large as a hen's Q^^. The choroid plexus is 
not infrequently the seat of transparent cysts, usually of small size ; 
they may contain a clear fluid, or colloid material, or droplets of fat, 
or calcareous particles. A small dermoid cyst containing hairs has 
been described. These cysts have no special pathological signifi- 
cance. 

Primary carcinomata are sometimes found in the ventricles. 



THE NP^RVOUS SYSTEM. 200 

The calcareous bodies called brain sand ' occur frequently in the 
choroid plexus (see Fig. 144), and corpora ainylacea may occur here 
and beneath the ependyrna. 

Cysticercus and echinococcus cysts are sometimes found free in 
the fluid of the ventricles. 

PINEAL GLAND. 

This little body, about the size of a cherry stone, is composed of 
connective tissue enclosing cavities, which are filled with reticulated 
tissue and round cells. The cavities often contain brain sand. It 
is said ^ that the pineal gland is an aborted or rudimentary organ 
and may be related to a median eye of invertebrate type. 

A small number of tumors belonging to the class of teratoma 
have been described as originating in the pineal gland. 

Weigert ^ describes a tumor, about 3^ cm. in diameter, composed 
of e2:>idermis, hair follicles, hair, sebaceous glands, cartilage, fat. 
smooth muscle, and cylindrical epithelium. 

Falkson^ describes a chondro-cysto-sarcoma, 5.8 cm. in diameter, 
which apparently originated in the pineal gland. 

Turner^ describes a tumor of the pineal gland, projecting into 
the third ventricle and the left lateral ventricle, of the size of a kid- 
ney. The tumor was composed of fusiform cells, of nerve ganglion 
cells, of tubules and acini lined with cylindrical epithelium, and of 
more irregular spaces filled with large polygonal cells. 

Coats" describes a tumor, three inches in diameter, groA\4ng into 
the third ventricle, the aqueduct of Sylvius, and the fourth ventricle. 
It was composed of fusiform cells, of tubules lined with cylindrical epi- 
tliehum, of irregular masses of epithelium, of cartilage, and of smooth 
muscle. 

THE PITUITARY BODY. 

This structure, called the Hypophysis cerebri, consists of two lobes. 
The anterior lobe is composed of a connective-tissue stroma enclosing 
cavities which are packed full of nucleated cells of various sizes and 
shapes, some of them resembling nerve cells. The posterior lobe is 
composed of va,sculai' connective tissue. 

Weigert^ describes a tumor, as large as a hen's egg, which rosoni- 

' The little, hard masses called /^/vr/'/i .<Jfr/n7 consist of airgrcii-ations of small parti- 
cles of carbonate and phosphate of lime, with a very small amount of phosphate of 
ammonia ami magnesia. With these there is more or less organic matter. 

- Quarterly Jour, of INIicr. Science, 18S6. 

^Virch. Arch., Ixv.. p. 213. -^Ibid.. Ixxv.. p. 550. 

''Trans, Lond. Path. Soc, xxxvi. ^Ibitl.. xxxviii. 

^Virch. Arch., Ixv., p. 219. 



300 THE NERVOUS SYSTEM. 

bled in its structure the normal anterior lobe of the pituitary body, 
and which he regards as a hypertrophy of that body. 

Weigert also describes a gummy tumor of the pituitary body as 
large as a hazelnut. 

Weichselbaum describes an adenoma of the pituitary body, as 
large as a pigeon^s egg, closely resembling the structure of the nor- 
mal anterior lobe of this body ; a small lipoma ; and a pituitary body 
with colloid cysts, lined with ciliated epithelium. 

THE BEAIN. 
THROMBOSIS AND EMBOLISM. 

In studying the occurrence and effects of thrombosis and embolism 
in the brain, certain peculiarities of the circulation should be borne 
in mind. The arteries of the brain are in part terminal arteries (see 
page 61), in part such as have anastomoses among their branches. 
Thus the arteries which are distributed to the cortical region form 
abundant anastomoses in the pia mater and are verv small when they 
enter the brain, while those which are distributed to the basal re- 
gion, and which supply the basal ganglia, are larger and do not, be- 
yond the circle of Willis, form anastomoses with one another. Thus 
it is that occlusions of the arteries supplying the basal ganglia are 
of much more serious import, aside from the importance of the parts 
involved, than those passing to the cortex. 

Thrombi may form in the arteries as a result of any degenerative 
or inflammatory process in the wall of the vessel leading to a rough- 
ening or death of its intima, or from pressure upon the vessel from 
without, or they may occur in vessels in whose walls we can detect 
no primary lesion. The most common causes are atheroma and 
simple endarteritis. Thrombi may also form around an embolus 
which does not entirely occlude the vessel. 

Emboli of the cerebral arteries most commonly arise from acute 
or chronic endocarditis or cardiac thrombi ; they may arise from 
aneurisms or atheroma of the aorta, from the carotid or vertebral 
arteries, or from the pulmonary veins. The materials constituting 
emboli vary greatly, depending on their mode of origin (see page 
61). The effects on the brain tissue of emboli and thrombi of the 
arteries are essentially the same in their main features. In some 
cases, however, in which large emboli, usually from endocarditis, 
suddenly block up a large vessel, the individual may die almost in- 
stantly without other apparent lesion than the stoppage of the vessel. 

In general, the first effect of the occlusion of an artery is to 



' Yirch. Arch., Ixxv., p. 444. 



THE NERVOUS SYSTEM. 



301 



deprive the region to which it is distributed of blood. In arteries 
whose branches anastomose, as in the cortex of the brain, the af- 
fected area is soon supphed with blood by the establishment of a col- 
lateral circulation. In terminal arteries, on the other hand, the 
blocking of the vessel is followed, as a rule, by degenerative changes 
and softening in the brain tissue. The appearances which these de- 
generated areas present vary greatly, depending upon the stage of 
the degeneration and the amount of blood which may be extra- 
vasated. Dense infiltrations of the brain tissue with blood, as in 
hsemorrhagic infarctions from emboli in other parts of the body, do 
not usually occur, although considerable blood may be extravasated. 




Fig. 154.— Degenerated Cells, Cholesterin Crystals, and Corpora amylacea from Brain 
Tissue in Embolic Softening. 

a, fatty ganglion cells; b, corpora amylacea; c, cell containing very large number of fat drop- 
lets (compound granular or Gluge's corpuscles); d, cholesterin crystals. 



Areas of softening in which there is little extravasation of blood 
are usually white or yellow in color {i chit e or ijcJJoir softening). 
When much blood is present the process is frecpiently called /•('(/ 
softening. The tissue in the affected area gradually softens ami 
may become diffluent. Microscopically, the softened tissue is seen to 
consist of more or less Huid with broken-down brain tissue, frag- 
ments of nerve fibres, droplets of myelin, nerve cells, shreds of 
neuroo:lia tissue and blood vessels, and red and white blood cells. 
Then evidences of degeneration are seen in the presence o( fat 



302 



THE NERVOUS SYSTEM. 



granules and droplets, larger and smaller cells densely crowded 
with droplets of fat (so-called Gluges corpuscles or compound 
granular corpuscles) (see Fig. lo-k). Various kinds of cells and cell 
fragments, more or less granular and fatty, and also corpora amyla- 
cea, blood pigment, fat crystals, and cholesterin crystals, may be 
found. The walls of the blood vessels may also be in a condition of 
fatty degeneration (Fig. 155). The color of the softened mass will 
of course depend upon the relative amounts of these elements. 

The tissue may remain for a long time in the soft condition, or it 
may be absorbed and replaced by a connective-tissue cicatrix which 
may be more or less pigmented ; or a wall of connective tissue may 
form about it, converting it into a well-defined cyst, with or without 
pigmented walls ; or the mass may dry and form a dense, structure- 
less nodule. Acute inflammatory changes may occur about the 




Fig. 155.— Blood Vessels from an Area of Embolic SoFTE>*ixa- of Braix. 
The -xalls of the vessels, particularly the endothelial cells, contain fat granules and fat droplets. 



dead tissue. In cases of infectious emboli numerous abscesses may 
be formed in addition to their mechanical action. 

Thrombi are most frequent in the internal carotids, less so in the 
middle cerebral, basilar, and vertebrals. They may occur, but still 
less frequently, in other cerebral arteries. Emboli are most common 
in the m.iddle cerebral artery, next in the internal carotid, and then 
in the basilar. The relative frequency with which embolism occurs 
in the middle cerebral artery is attributable to the directness with 
which the blood passes into this artery from the heart. The great 
significance attaching to embolism of the middle cerebral artery is 
evident when we remember th^t its branches are terminal arteries, 
and are distributed to such important structures as the lenticular and 
caudate nucleus, the internal capsule, and the optic thalamus. 



THE NERVOUS SYSTEM. 303 



HYPEREMIA AND AN.EMIA. 



The appearance of the brain tissue after death does not always 
furnish rehable indications of its blood contents during life, though 
they are perhaps more to be depended on than the appearance of the 
meninges. 

Some of the more common conditions determining hijpercemia 
which are mentioned above as influencing the meninges apjjly also 
to the substance of the brain. In sections of hypersemic brains the 
small blood points from the cut ends of small vessels are more nu- 
merous and conspicuous than under normal conditions, and the brain 
tissue, particularly the gray matter, may have a diffuse red color. 
If excessive the convolutions may be somewhat flattened, and the 
brain tissue and pia mater may be oedematous, and the ventricles con- 
tain fluid. The congestion of the vessels may be general or localized. 

Ancemia of the brain may be either local or general. It may de- 
pend upon a general ansemia or upon general disturbances of the 
circulation, such as mitral stenosis or regurgitation ; or upon local in- 
terference with the arterial blood supply, such as complete or partial 
obstruction of the arteries from thrombi, emboli, inflammatory 
changes, spasmodic contractions, etc., or from tumors, exudations, 
and blood extravasations pressing upon the vessels from without. 
In oedema of the meninges, and in the presence of internal hydro- 
cephalus, the brain tissue is apt to be anaemic. The brain tissue in 
ansemia looks whiter than usual, the contrast between the gray and 
white matter is less marked, and the small blood points usually seen 
on section from divided vessels may be very inconspicuous or almost 
entirely absent. 

CEDEMA 

of the brain tissue may accompany either hypersemia or anaemia, 
and seems in most cases, though not always, to be dependent 
upon conditions which induce these alterations in the blood con- 
tents of the brain. In some cases of marked impoverishment of the 
blood a so-called liyclrcemic oedema of the brain is found. Very 
marked oedema of the brain may exist without any accompanying 
brain symptoms. On the other hand, persons may die comatose ; 
this is seen with especial fre^iuency in acute and chronic alcohol 
poisoning, but may occur under other conditions, and the post-mor- 
tem examination reveals nothing but anlema of the brain tissue, 
either with or without anlema of the pia mater. 

H.EMORKHACE. 

HiX3morrliages in the substance of the brain may be vorv small 
and punctate, and are then usually called atpi/htrt/ hivmorrhafjis : 



304: THE NERVOUS SYSTEM. 

or they may result in the collection in the brain tissue of masses of 
blood of considerable size, which are called apoplectic foci or clots. 
These forms of haemorrhage may be associated, or a number of 
capillary haemorrhages may join to form an extensive clot. 

Capillary hcemorrhages may look, on section of the brain, like 
the severed ends of hypersemic blood vessels, or the tissue about them 
may be more or less tinged with blood. Microscopically, the peri- 
vascular spaces will be found distended mth blood, which may have 
escaped into them and more or less broken down the brain tissue. 
They may occur singly, but are frequently multiple, so that the brain 
tissue is besprinkled with blood points. Degeneration of the extra- 
vasated blood may give rise in later stages to reddish or brown or 
yellowish circumscribed discoloration of the brain tissue, due to gran- 
ules and crystals of blood pigment intermingled with broken-down 
brain tissue, with more or less fatty degeneration of its elements. 
Capillary haemorrhages may be due to fatty degeneration of the ves- 
sels leading to rupture ; or the extravasation may be due to diape- 
desis, or it ma}- depend upon conditions which we do not understand. 
They frequently occur in the vicinity of apoplectic clots and tumors , 
they may be due to thrombosis of the veins or of the sinuses of the 
dura mater ; they not infrequently occur in acute encephalitis, in 
congestive hypersemia, in acute mania, and in delirium tremens ; 
and they may be associated with general diseases, such as scurvy, 
purpura hsemorrhagica, typhus fever, pyaemia, ulcerative endocar- 
ditis, etc. ; they may be associated with embolic softening. 

Apoplectic foci may result from the coalescence of numerous 
capillary haemorrhages ; from injury, or from rupture of diseased ar- 
teries, either with or without changes in the blood pressure. Haem- 
orrhages from injury to the skull may occur as well without as with 
fracture, and may be situated over the vertex as well as at the base 
of the brain, and vary in extent and seat, depending upon the cha- 
racter and point of the injury and the size of the vessels involved. 
The so-called spontaneous haemorrhages, other than those of capil- 
lary origin, which give rise to masses of blood and broken-down 
brain tissue, may vary in size from that of a pea to those occupjang 
a large part of a hemisphere. They are due, in a very considerable 
proportion of cases, to the rupture of small arterial aneurisms, but 
may arise from weakening of the walls of the arteries, from arteri- 
tis, atheroma, or fatty degeneration. These latter forms of disease 
doubtless give rise in most cases to the formation of the aneurisms 
whose rupture is in so many cases the immediate cause of the heem- 
orrhage. Aneurisms of the cerebral arteries may be as large as a 
pea or hazelnut, but those most frequently met with and causing 
apoplexy are usually small — called miliary aneurisms — and may be 



THE NERVOUS SYSTEM. 305 

microscopic in size, varying from this up to that of a largo pint's 
head or larger. They may be sacculate or fusiform, and frequently 
exist in considerable numbers. They may occur in any of the small 
arteries of the brain, but are said to be most frequent on the branch • 
es of the middle cerebral artery. It is asserted that the bursting 
of miliary aneurisms is the nearly if not quite exclusive cause of the 
formation of spontaneous apoplectic clots, but this we do not be- 
lieve to be true. As to the immediate cause of rupture, either of 
aneurisms or otherwise diseased blood vessels in the brain, we are in 
many cases entirely ignorant. In some cases it seems to be due to 
an increased arterial tension in such diseases of the heart as induce 
this change, as in the cardiac hypertrophy which may accompany 
some forms of chronic diffuse nephritis ; or it may result from un- 
usual exertion or mental excitement ; but, as above stated, in many 
cases the immediate inciting cause is not evident. 

The most frequent seat of hsemorrhage is in the corpora striata 
and optic thalami, and the brain tissue in their A^cinity, and here 
they occur most often in the parts supplied by the branches of 
the middle cerebral artery. The possibility of hsemorrhage in the 
floor of the fourth ventricle as a cause of sudden death should be 
borne in mind in investigating cases of sudden death from obscure 
causes. 

Haemorrhages frequently seriously affect other portions of the 
brain than those immediately supplied by the ruptured vessels. 
Thus haemorrhages in the cortical substance or beneath the pia mater 
may force their way deep into the brain substance ; or, in haemor- 
rhage in the brain substance, the blood may burst into the ventricles 
or work its way into the intermeningeal space, and, either at the seat 
of its occurrence or in the situations into which it is forced, it may 
give rise to serious compression of the brain. Portions of the brain 
containing large extravasations may be enlarged, the tissue anaemic 
from pressure, the convolutions flattened, and the surface dry. As 
the blood is poured out the brain tissue is usually torn and lacerated, 
so that the apoplectic clot usually consists of detritus of brain tissue 
intermingled with blood. If, however, the blood is poured out from 
a single vessel, the lacerated brain tissue maj- be pressed aside, and 
the greater portion of the red mass m<vy consist of pure blood clot. 

The appearances presented b}' hannorrhages in the brain vary 
greatly, depending upon the time Avhich has elapsed since their occur- 
rence. If life continue, the anlenia which usually soon occurs in the 
vicinity of the hiBmorrhage disappears and tlie clot becomes drier 
and firmer ; gradually the blood undergoes the usual series of 
changes seen in extravasation : the luenioglobin decomposes, form- 
ing granules and crystals o( blood pigment : the blood colls ami 



306 THE NERVOUS SYSTEM. 

fibrin undergo degeneration and absorption ; the detritus of brain 
tissue undergoes fatty degeneration. As these alterations occur the 
color changes to reddish-brown, orange, or yellow, and the adjacent 
brain tissue may be discolored by imbibition. 

Inflammatory reaction may occur in the vicinity, leading either 
to the formation of a more or less pigmented cicatrix, or to a cyst 
with yellowish fluid contents and a fibrous, more or less pigmented 
wall. The process of degeneration and absorption of the blood and 
broken-down brain tissue, and their replacement by a cyst or by a 
cicatrix, is a slow one, and the cysts and cicatrices may resemble 
those formed at the seat of embolic softening. Not infrequently we 
find in the brain of a person dead from recent apoplexy the remains 
of old clots presenting some one of the above-described stages of ab- 
sorption. The apoplectic cysts and cicatrices persist for a long time 
after their formation. 

SECONDARY DEGENERATIONS. 

Lesions of parts of the brain which involve the destruction of 
brain tissue containing certain systems of motor nerves, owing, it is 
believed, to the separation of these nerves from their trophic centres, 
are regularly followed after a time by degenerative changes in these 
nerves below the seat of lesion. It is particularly lesions in the 
central convolutions, the internal capsule, portions of the corona 
radiata, and the pes pedunculi, which destroy the motor fibres pass- 
ing through these parts, and are follov^ed by degenerative changes 
in the fibres below. The most important and frequent lesions fol- 
lowed by this effect are those involving the anterior two-thirds or 
three-fourths of the internal capsule. It will suffice merely to men- 
tion these changes here, as they are considered more in detail in the 
section devoted to lesions of the spinal cord. 

HYPERTROPHY AND ATROPHY OF THE BRAIN. 

True Hypertrophy of the brain is rare, and probably always 
congenital. An increase in the size of the brain from the prolifera- 
tion of the neuroglia sometimes occurs in children either before or 
after birth, less frequently in youth, and very seldom in adults. 
The white substance of the hemispheres is increased in amount. If it 
takes place before the ossification of the cranium, the bones are sepa- 
rated at the sutures and fontanelles ; if after this, the inner table of 
the skull may be eroded and thinned. When the cranium is opened 
the dura mater appears tense and ansemic, the convolutions of the 
brain are flattened, the brain substance is firm and ansemic, the ven- 
tricles are small, the ganglia and cerebellum are either of normal 
size or compressed. 



THE NERVOUS SYSTEM. 307 

The disease is usually very chronic, and destroys life with symp- 
toms of compression of the brain. There may, however, be acute 
exacerbations. 

Atrophy. — This may occur as a senile change, or, in adults, in 
chronic alcohol, opium, or lead poisoning, in chronic insanity, and 
in chronic meningitis. In children who are much reduced hj chronic 
diseases atrophy of the brain may accompany atrophy of the rest of 
the body. 

The atrophy affects principally the cerebral hemispheres, and may 
be uniform or more marked in some parts than in others. The con- 
volutions are small, the sulci broad, the ventricles usually dilated, the 
brain tissue firm, the gray matter discolored, the white substance 
grayish in color ; the blood vessels may be dilated. The basal gan- 
gha may be small. Serum accumulates in the pia mater and the ven- 
tricles ; the pia mater, and often the skull, become thickened ; the 
brain tissue may be oedematous or contain small haemorrhages. The 
nerve elements of the brain tissue are those most involved in the 
atrophy. 

WOUNDS OF THE BRAIN. 

The brain may be directly wounded by a foreign body, or indi- 
rectly by fragments of bone driven into it, or it may be lacerated by 
severe contusion without fracture or solution of continuity of the 
skull. It is very difficult to estimate the degree of injury which 
must cause death, since persons frequently die from slight, and may 
recover from very severe, wounds of the brain. In incised wounds of 
the brain more or less haemorrhage occurs at the seat of lesion, and 
the brain tissue in the vicinity soon undergoes degenerative changes. 
These may be comparatively slight or extensive. Inflammatory re- 
action may occur in the vicinity, and the adjacent brain tissue, as 
well as the hsemorrhagic and degenerated area, become intiltrattnl 
with pus cells. After a time the injured and degenerated area may 
become surrounded by new-formed connective tissue, and the de- 
composed extra vasated blood and detritus of brain tissue, nu>rt^ or 
less fatty, may be absorbed, and thus after a time the part heals by 
a more or less pigmented cicatrix. The healing is in most cases very 
slow and may occupy months or even years. The pia mater may 
participate to a marked degree in the intlannuatory healing process. 
Abscesses may form near the seat of injury. 

After wounds which involve the removal o^ portions of tluM'ni- 
nial bones, it is not uncommon after a few d.iys to see a bKH^ling 
fungous mass })roject throiigii the oj)eniiig. This mass, some- 
times wrongly calUnl hernia cerebri, consists o( degeniM-atinl brain 
tissue, blood, and granulation tissue, ^vitll nioiv^ or less pus. Tlie 



308 THE NERVOUS SYSTEM. 

"brain tissue below it is degenerated, broken down, soft, and puru- 
lent, and there is often abscess in the adjacent brain tissue. Such 
w^ounds may finally heal by the absorption of the broken-down brain 
tissue and blood, and its substitution by granulation tissue. 

Lacerations of the brain tissue without fracture may appear 
shortly after the injury as simple more or less circumscribed areas 
of capillary hsemorrhage ; the brain tissue about these may degene- 
rate, pus may form, and abscesses be developed ; or the degenerated 
and lacerated tissue may be gradually replaced by granulation tis- 
sue which finally forms a cicatrix. The process of degeneration 
and softening and of healing in such lacerations of brain tissue may 
occur very slowly indeed, even occupying years, and not infre- 
quently the degenerative changes are very extensive and progres- 
sive. In many cases, of course, the injury is so extensive, or in- 
volves such important parts of the organ, that very Uttle or no 
nflammatory or degenerative change takes place before death. 

HOLES OR CYSTS IN THE BRAIN. 

Larger and smaller holes may be found in the brain tissue from 
dilatation of the perivascular lymph spaces, or well-formed cysts 
may exist from hsemorrhage, inflammatory softening, hydatids, etc. 
There are, however, cases in which one or several holes of varjdng 
size are found in the brain which cannot be determined to have 
either of the above raodes of origin. They may lie deep in the brain 
substance or close under the pia mater, or may communicate with 
the ventricles. This condition is sometimes called porencephalies 
and may co-exist with various mental aberrations, hydrocephalus, etc. ^ 

INFLAMMATION OF THE BRAIN (ENCEPHALITIS). 

It has been already mentioned that the brain tissue about haemor- 
rhages and areas of embolic and thrombotic softening may undergo 
inflammatory changes leading to the formation of new connective 
tissue. There is a class of cases in which localized areas of the brain 
undergo softening, with more or less extravasation of red and white 
blood cells and hyperemia of the blood vessels, so that the softened 
material consists, as seen under the microscope, of detritus of brain 
tissue in a condition of fatty degeneration, with more or less pus 
cells or pigment. When such areas are red in color from inter- 
mingled blood cells or pigment the condition is called red inflam- 

1 Consult Kundrat, "Die Porencephalie," Graz, 1882 ; and Savage and White, 
*' On the Causes of Holes in the Brain," Trans. London Path. Soc, vol. xxxiv., p 1, 
1883. 



THE NERVOUS SYSTEM. 301> 

matory softening. When fatty degeneration prevails, and the red 
blood cells or their derivatives are not abundant, the softened area 
looks yellow or yellowish- white, and this is often called yelloiv in- 
flammatory softening. The origin of these processes is very ob- 
scure and their inflammatory nature not well defined. 

Abscess of the Brain. — The small multiple abscesses of the brain 
which occur with pysemia form part of that disease and require no 
separate description. 

The large single abscesses occurring under different conditions 
are those to which the name of ^^ abscess of the brain ^Ms usually 
applied. 

These abscesses occur in two forms : 

The non-capsulated abscess, an irregular cavity containing thin 
pus and softened brain tissue. The walls of the cavity are ragged 
and infiltrated with pus, and outside of the walls is a zone of oede- 
matous and softened brain tissue. If the abscess is near the pia ma- 
ter it may set up a meningitis ; if it is near the lateral ventricles it 
may rupture into them ; if it is near the sinuses of the dura mater it 
may cause thrombosis. 

The encapsulated abscess has a capsule of connective tissue, and 
contains thin or cheesy pus. 

Abscesses of the brain are usually single : they may attain a con- 
siderable size. They are most frequent in the cerebral and cere- 
bellar hemispheres, rare in the central ganglia, the pons, and the 
medulla oblongata. 

The most common cause of this disease seems to be chronic sup- 
purative otitis (42.5 per cent, Gowers), while acute otitis is a com- 
paratively rare cause. With the otitis there may also be caries of 
the temporal bone, suppuration of the mastoid cells, and inflamma- 
tion of the dura mater. The abscess is usuall}" situated deep in the 
brain ; only rarely is it continuous with the inflamed dura mater and 
bone. When the abscess is deeply situated, and the bone and dura 
mater are not diseased, it is difficult to tell lunv the infection travels 
from the ear to the brain. Abscesses due to this t'.uise are situated 
in the temporo-sphenoidnl, the frontal, tlie occipital, and the parie- 
tal lobes, or in the cerebellum. 

Another frecpient cause of abscess of the brain is traumatism — 
blows or falls on the head {'l\ per cent, Gowers). Sucli injuries may 
not hurt the skull, or may pn)duce fracturt^s or lUHTosis. There is 
often a considerable interval bc^twiHMi \\\o time when th^ injury i< 
inflicted and that when the symptoms ot the abscess are developeil. 

Wlien the cranial lH)nes are nninjured the abscess is situated di\^p 
in the bi-ain : avIumi t1uM-i^ is necrosis of tlie bones the absct^s^^ may 
be superficial ; when the bones are fractured the abscess may bo 



310 THE NERVOUS SYSTEM. 

either superficial or deep. The abscess is regularly situated beneath 
the point of injury, rarely in the opposite side of the brain. 

Chronic disease of the nose, either the mucous membrane or the 
bones, has been the cause of a few abscesses in the frontal lobes. 
Disease of the orbit has also given rise to abscesses in the same 
position. In a few cases the abscesses have been due to caries of 
various portions of the cranial bones. 

In a considerable number of cases (one-sixth, Gowers) no cause 
for the abscess has been discovered. 

Very frequently in acute meningitis there is an infiltration of pus 
cells along the walls of the vessels which enter the brain from the 
pia mater ; and under a variety of conditions which we do not un- 
derstand, as in some cases of typhoid fever, delirium tremens, ery- 
sipelas, and under many other conditions, there are numerous and 
sometimes very large numbers of leucocytes scattered through the 
substance of the brain, sometimes around the ganglion cells, some- 
times along the vessels in the perivascular sheaths. 

Chronic Interstitial Encephalitis — Sclerosis. — This lesion of 
the brain tissue may occur diffusely, occupying an entire lobe or 
more or less of the ^whole brain, or in circumscribed small areas. It 
consists essentially in an increase of the connective-tissue elements, 
the neuroglia, and an atrophy of the nerve elements, particularly the 
ganglion cells and the medullary sheaths of the nerves. With these 
changes are usually associated the formation of Gluge's corpuscles, 
corpora amylacea, granular and fatty degeneration of the nerve ele- 
ments, and thickening and proliferation of cells of the walls of the 
blood vessels. The areas of sclerosis may be very dense and hard, 
or gelatinous in consistence. 

The diffuse form of sclerosis is most frequently seen in general 
paresis of the insane, and not infrequently in the brains of drunk- 
ards. 

The circumscribed form of sclerosis, multiple sclerosis {sclerose 
en plaque), is much more common than the diffuse form, and may 
occur in the brain alone, or may be associated with a similar lesion 
in the spinal cord. It is almost entirely confined to the medullary 
substance, and the areas of sclerosis vary in size from that of a pea 
to that of an almond. They may be few or numerous, they may be 
white, gra}dsh, or grayish-red in color, and are usually, but not 
always, sharply outlined against the unaltered brain tissue. Al- 
though in many cases the increase in the connective-tissue elements 
seems to be the primary lesion, and the degeneration of the nerve 
elements secondary to this, it is quite possible that in some cases the 
increase in connective tissue may be secondary to a degeneration of 
the nerve elements from loss of nutrition or from other causes. 



THE NERVOUS SYSTEM. 



311 



Encephalitis in the New-horn. — This condition, first described 
by Virchow, is said to consist in the formation of circumscribed col- 
lections of cells of various sizes containing many fat granules (granu- 
lar corpuscles) and forming yellowish masses, from 1 mm. to 6 mm. 
in diameter, in the brain tissue. A more diffuse occurrence of granu- 
lar corpuscles is also described, but this is said by some observers to 
be physiological. The nature of this lesion is but little understood 
and is still the subject of controversy. 

Syphilitic Inflammation of the Brain sometimes results in the 




wm 






.>^^ 






H- 







i 




— <^ 



/ 



y 



Fia. 156.— SYPniLiTio Obliterating Endarteritis of a Cerebral Artery. \ SOaud rx\luoi\l. 

formjition of so-c^allod gummy tumors. Those are most frequently 
fouiul near the periphery of the brain, not infrotpiontly comuvtod 
Aviih the meninges, and may be sharply circumscribtHl. The ivntral 
portion of the tumor is usually in a c^Mulitiou of clieesy degeneration. 
a,nd in the ])erip]uM-y we see fibrous tissue or a dense infiltration of 
small s})heroidal cells. 

Syphilitic inflannnation o( the brain very frtHpientlv oi\*urs in 
aditfiiso form, characterized by the formation of a gelatinous, uravish 



312 



THE NERVOUS SYSTEM. 



tissue consisting of a more or less homogeneous or granular base- 
ment substance, with numerous small spheroidal cells. The nerve 
elements are atrophied. Obliterating endarteritis may occur as a re- 
sult of syphihtic poisoning (Fig. 156). 

Tubercular Inflammation of the brain substance usually mani- 
fests itself in the formation of circumscribed masses of new tissue 
from 0.5 cm. to 1 cm. in diameter, or larger. These may be single 
or multiple, are most common in young persons, and very fre- 
quently occur in the cerebellum. They are apt to occur in connec- 
tion with tubercular inflammation of other organs. They are fre- 
quently called solitary tubercles, and usually consist of a dense 















"^m 



ife^ 






•i^--^-^' 




^y^ 



Si- 



Fig. 157,— Solitary Tubercle of Cerebellum. 
(7. a, miliary tubercles with giant cells; b, b, miliary tubercles without giant cells; c, diffuse 
tubercle tissue; d, central cheesy mass; e, nerve tissue of the cerebellum. 



central cheesy mass, around which is a grayish zone containing 
tubercle granula, numerous small spheroidal cells, with occasionally 
larger polyhedral cells and giant cells (Fig. 157). They do not, as 
a rule, seem to be formed by an aggregation of miUary tubercles, 
although these may be present in the periphery. Tubercle baciUi 
have been found in these solitary tubercles. 

They sometimes suppurate and break down, and then may simu- 
late simple abscesses. 



O 1 o 



THE NERVOUS SYSTEM. .]]/, 

Conglomerate and scattered miliary tubercles of the ordinary 
form sometimes occur in the brain, usually in connection with tuh>er- 
cular inflammation of the meninges or ependyma. 

LESIONS OF THE BRAIN IN GENERAL PARESIS OF THE INSANE. 

The changes in this disease are in the main those of chronic dif- 
fuse encephalitis, but the appearances vary greatly and depend to 
some extent upon whether the brain is examined in early or late 
stages of the disease. According to Meyer, in the early stages of the 
disease the convolutions, particularly of the anterior cerebral lobes, 
are swollen, the gray matter congested and softened in 2:>laces. The 
brain tissue is more or less infiltrated with leucoc}i;es. Fatty de- 
generation of the walls of the capillaries, and punctate hsemorrhages, 
are also common. 

In later stages of the disease a great variety of changes may be 
observed : hsemorrhagic j^achymeningitis, thickening of the dura 
mater, and close adhesions to the skull ; thickening and opacities of 
the pia mater, adhesions of the latter to the dura mater and to the 
brain tissue. The brain tissue is apt to be atrophied, and the ventri- 
cles dilated and filled with fluid. The pia mater may be oedematous, 
the ependyma thickened and roughened. On microscopical exami- 
nation the neuroglia is found to be increased in amount, the ganglion 
cells shrunken and sometimes pigmented ; the nerve fibres ma}' also 
be atrophied, and the blood vessels in a condition of fatty or hyalin 
degeneration. There may be an accumulation of fatty and granular 
cells along the walls of the blood vessels. Secondary degenerations 
in the spinal cord are not infrequently observed. 

It is very difficult to make positive and definite statements regard- 
ing many such lesions of the brain as those just indicated, or in 
general of brain lesions whose nature must be revealed b}' microsco- 
pical study, because our technical procedures in the study of the 
brain, even in normal conditions, arc still quite unsatisfactory and 
incomplete. The brain tissue is so delicate and liable to post-nu>rtom 
changes, and the effects of different preservative agents are so liable 
to valuations, that great caution is necessary in arriving at conchi- 
sions regarding the minuter lesions affecting the nerve tissue o( tlie 
brain. 

PKiMENTATTON. 

This may occur in any })ortit)n o\' the brain ov its meninges (voin 
tl\(^ d(H'onq)()siti()n ef extravasated blood. In jXMsons at1\»eted by 
malaria. fh(> gray niattiM* oi' the lu-ain has S(Mnt>linii\s ;ni unusually 
(lark ov own blackish appearand^ This ei^K>r is due to the ]>restMiee 
o\' black pigment granules within tlu^ capillary blood vessels. The 
'jS 



314 THE NERVOUS SYSTEM. 

obstruction to the vessels by masses of these pigment granules may 
cause capillary apoplexies. The pigment may also be found in the 
walls and in the lumina of the vessels of the pia mater. 

Pigmented patches of congenital origin are not infrequently seen 
in the pia mater. They may be due to the presence of branching 
pigmented cells. 

TUMORS OF THE BRAIX. 

« 

Xeuroglioma ganglionare. — This is a form of tiunor probably 
due to disturbances in the development of the brain. It occurs in 
the form of circumscribed tumors or of diffuse enlargements of por- 
tions of the brain. The pia mater over these tumors is unchanged 
and the convolutions retain their shape. The tumors are formed of 
neuroglia, in "which are contained little grouj^s of ganglion cells 
(Ziegler). 

Glioma. — This is the most common tumor of the brain. It occurs 
vdth especial frequency in children and young adults. Such tumors 
occur in all parts of the brain, but they are found most frequently in 
the cerebrum. There may be a single tumor, or there may be sev- 
eral such tumors in different parts of the brain ; some of them attain 
a large size. These tumors may be sharply circumscribed, or merge 
imperceptibly into the brain substance ; sometimes the tumor is ar- 
ranged so as to form the "wall of a cyst which contains clear serum. 
They may be white and hard : gray, soft, and gelatinous ; infiltrat- 
ed with small hsemorrhages ; or partly degenerated and softened. 
The brain tissue around these tumors may be inflamed or necrotic. 
The tumors are composed of neurogha, the relative quantity of neu- 
rogha cells (Fig. 120) and of fibrils (Fig. 119) varying in the different 
timiors. 

If the cells are very numerous, with but little basement sub- 
stance, the tumor is called a giio-sarcoma. 

Sarcomata occur in any part of the brain. They are single or 
multiple. They are composed of round or fusiform cells ^vith more 
or less basement substance. 

Eiidotlieliomata are found in the substance of the brain. They 
are of the same tyj)es as have been described as occurring in the 
pia mater. 

Myxoma, fihroma, lipoma, and osteoma are rare forms of brain 
tumor. 

Angioma. — Small collections of dilated vessels are found in the 
substance of the brain. They seem to be congenital, like the nse^4 
of the skin. 

The cysts of the cerebellum are very curious bodies. They are 



THE NERVOUS SYSTEM. 31 

found in young persons and in adults. They occur in any one of the 
lobes of the cerebellum. They may be as large as a hen's e^^^f^. They 
contain clear serum or colloid matter, and their walls are formed of 
thickened neuroglia. We are ignorant of their mode of origin. 
They give marked clinical symptoms and are regularly fatal. ^ 

PARASITES. 

Cysticercus and, more rarely, echinococci are found in the brain. 

MALFORMATIONS. 

Cyclopia. — This malformation consists in an arrest of develop- 
ment affecting the cerebrum, which, instead of separating into two 
hemispheres, remains single, with one ventricle, and the rudiments 
of the eyes usually become joined and form one eye. This single 
eye is in the middle of the face, near the place of the root of the 
nose, in a single orbit. Over this is an irregular body representing 
the nose. The rest of the face is well formed. Or the eyeball may 
be wanting entirely, or there are two eyes joined together, or, more 
seldom, two separate eyes. The orbit is surrounded by rudiments 
of four eyelids. The frontal bone is single, the nasal bones unde- 
veloped ; the ethmoid, vomer, and turbinated bones are absent. The 
optic nerve is double, single, or absent. There may be hydrocepha- 
lus. Such children are incapable of prolonged existence. 

Anencephalia. — This malformation may be of various degrees. 
The brain may be entirely absent, and the base of the cranium is 
covered with a thick membrane, into which the nerves pass. Or the 
membranes may form a sort of cyst containing blood and serum, (^r 
portions of brain. Of the cranial bones, only those Avliich form the 
base of the skull are present (Acrania). The scalp is usually partly 
or entirely absent over the opening in the skull ; the 03'es stand 
prominently out, and the forehead slopes sharply backward. This 
malformation may occur in otherwise well-developed children. 

Hydrocephalus. — This lesion has been already considered on page 
21)7. It is probable that in some cases Jn/droccphahis in fern us is due 
to a primary joayfm/ aueiiaphalia, mul that the accumulation of 
fluid is of secondary occurrence. In rare cases, only j^irt of one lateral 
ventricle is hydrocephalic, giving to ihi^ head a i)rotuheraiu'e on t^ne 
sid(\ Tlie viability of the fd^tiis depends upon tlie degree ot* the 
liydroc(\phalus. 11 ydroccplnf/us c.rfcrHNs is an aeeunmlatiou of 
scn'um b(^n(^n.th the pia. mat(M-, or, .u'coiHliiig to some authors, between 
Ihepiaaiid dura, mater, it caiist^s dilatation of the t'ranium and 
i'ompressioii of (lu^ bi-ain. It is ol' very rare oeeurrenee, and may 
also be seeoiulary to partial aiuMioi^phalia. 



'Trans. I.oiul. Path. Soc. xli. 



316 THE NERVOUS SYSTEM. 

Cephalocele, or Brain Hernia. — When abnormal openings exist 
in the skull from malformation, the contents of the cerebral cavity 
are apt to protrude in the form of larger or smaller sacs. This may 
occur in cases of well-marked anencephalia or in cases in which the 
brain is well developed. The protruding sac formed of the meninges 
may or may not be covered with skin. If the contents of the sac 
are simply fluids the lesion is called liydr omening ocele ; if composed 
of brain substance, enceplialocele ; if the sac contain both fluid and 
brain substance, it is called liydrencephalocele. The sacs may be 
very small or as large as a child's head. They may protrude from 
the top of the skull in acrania. They most frequently protrude 
through openings in the occipital bone, often hanging down in large 
sacs upon the neck ; also at the root of the nose, along the line of the 
sutures, at the base of the skull, and elsewhere. 

Microcephalia. — This is an abnormally small size of the brain, 
with a correspondingly small cranium. The diminution in size af- 
fects principally the cerebral hemispheres, though the other parts of 
the brain are also small. The convolutions are few and simple, the 
cavities often dilated with serum ; on the membranes there may be 
traces of inflammation. The cranium is small, the face large, the 
rest of the body small. The malformation is ir some cases caused 
by inflammation or dropsy of the brain during fcBtal life. It is en- 
demic in some countries, but single cases may occur anywhere. The 
foetus is viable. Absence or incomplete development of portions of 
the brain may occur, not only in idiots, but in persons whose minds 
are perfect. 



THE SPIISrAL COED. 



THE MEMBEANES OF THE SPINAL CORD. 

A.— THE DURA MATER SPINALIS. 

The dura mater spinalis, unlike that cf the brain, does not serve 
as periosteum to the bones forming the cavity, so that the lesions 
of the two membranes differ somewhat. 



HAEMORRHAGE. 

Haemorrhage may occur, as the result of injury, between the dura 
mater and periosteum, or it may occur in tetanus, as a result of circu- 
latory changes induced by muscular spasm, or in the asphyxia of 
new-born children. Small hsemorrhages on the surfaces of the mem- 
brane may occur as the result of inflammation. 

Serous fluid may accumulate outside of the dura mater as a re- 
sult of post-mortem changes, or in connection with circulatory or 
inflammatory changes in the membranes. 

INFLAMMATION. 

Acute external pacJti/nieniiKj/'fi.s is usually secondary to dis- 
ease or injury of the spinal column, and may result in collections 
of pus between the dura mater and periosteum, usually most abun- 
dant posteriorly. Hivniorrhaqic pnvlnpneuiiujitis occurs in thr 
dura mater spinalis, with the formation of products similar to tln»«' 
observed in the brain, in the chronic insane ami in drunkards. 5/;//- 
ple chronic p((cln/ntenin(/i( is iuicnin, with the formation of new 
connective tissue containing brain saml, is not infreipuMit. Thr 
new (issue may form niiniili^ projections ov rtuighnoss of the sur- 
face, or, whcMi more abundant, llu^ psannuonntta. Tubcrculr in- 
jianniml ion o'i the dura, niator spinalis may occur in I'onniH'tion ^vith 
tuluM'cular nuMiingitis, ov W^ secondary to tnbiM-cular intlammatioii 
of the vertebriB. 



318 THE SPINAL CORD. 

TUMORS. 

Fibromata, lipomata, chondromata, myxomata, endotlie- 
liomata, and adeno-sarcomata ' occur in the dura mater spinalis 
as primary tumors. Carcinomata and sarcomata may occur as 
secondary tumors. Small plates of new-formed hone are rarely 
found in the dura mater spinalis. 

PARASITES. 

Echinococcus developing outside of the spinal canal may perfo- 
rate the dura mater ; or the cysts may lie between the dura mater 
and the pia mater. 

It is obvious that even small tumors in the spinal canal may give 
rise to serious results from compression. 

B.— THE PIA. MATER SPINALIS. 

It is almost impossible in most cases in the pia mater, as well as 
in the dura mater spinalis and in the spinal cord, to judge with cer- 
tainty, from the appearances after death of the blood contents of the 
vessels, of these parts during life. The same is true of abnormal 
quantities of serum found after death. The veins of the pia mater, 
especially in the posterior region, may be greatly distended with 
blood after death, without pre-existing disease ; and the intermen- 
ingeal space may contain much fluid under the same condition. 

HEMORRHAGE. 

Haemorrhages may occur from injury in connection with severe 
convulsions, or general diseases such as the hsemorrhagic diathesis, 
scurvy, small-pox, etc. The haemorrhages under these conditions, 
except from injury, are not usually extensive. But in some cases 
of injury or cerebral apoplexy ; from the bursting of aneurisms of 
the basilar or vertebral arteries ; or in cases in which we cannot find 
a cause, a very large quantity of blood may collect between the dura 
and pia mater, and in the meshes of or beneath the latter. 

INFLAMMATION. 

Acute exudative spiual meningitis occurs under essentially the 
same conditions and with essentially the same post-mortem ap- 
pearances as acute cerebral meningitis, though it is less frequent. 
The exudations are apt to be most abundant in the posterior por- 
tions. It may be associated with a similar inflammation of the pia 

' Hodenypl, American Journal of the Medical Sciences, March, 1888. 



THE SPINAL COKD. 'MU 

mater cerebralis, and the inner surface of the dura mater ma\- be 
involved. The disease may he circumscribed, but usually affects 
the entire length of the membrane. 

Tubercular inflammation is usually most marked, when asso- 
ciated with a similar condition of the pia mater cerebralis, in the uy- 
per portions of the cord ; but it may extend over the entire membrane. 
The conditions under which it occurs and the character of the le- 
sions are similar in both. Chronic spinal meningitis is not infre- 
quent, manifesting itself in the formation of larger or smaller 
patches of new connective tissue or thickenings of the pia mater. 
The pia and dura mater may thus be firmly united in places by ad- 
hesions, or the pia mater may become closely adherent to the sulj- 
stance of the cord. 

Not very infrequently large numbers of pigment cells are found 
in the pia mater spinalis, sometimes giving it a distinct gray or 
blackish color. 

TUMORS. 

Small plates of cartilage and hone are sometimes found in the 
pia mater. 

Fibromata, myxomata, sarcomata, and endotheliomata have 
been found. 

PARASITES. 

Cysticercus sometimes occurs in the meshes of the pia mater. 

THE SPINAL CORD. 

HAEMORRHAGE. 

This is much less frequent than in the brain, but may occur 
either as capillai^y apoplexy or as larger apoplectic clots. Cai>il- 
lary ha3morrhages, similar in appearance to those of the brain, ma}' 
occur as the result of injury, or near areas of softening or tumoi*s, or 
may accompany severe convulsions, as in tetanus. Apoplectic clots, 
which are comparatively rare in the spinal cord, are usually small, 
commonly not more than one cm. in diameliM-, and are similar in 
their appearances, and in the changes subseipient io their forma- 
tion, to those of the brain. They are usually the result of injury : 
but they may occur spontaneously. ])robably in most casi^s a^ a result 
of inliainmation, and nvo tlu^i most apt to oonir in the uiay niattor. 
Sometimes, liowevtM", haMiiorrhagic foci :\vo touiul in the spinal cord 
Avitliout traumatism or e\i(lence o( iiitlaininatory rhan^w 

I N.I ri: IKS. 
The spinal cord may be coini>ress(>il oi- hu'iM-attnl by juMietratiuix 



320 THE SPINAL CORD. 

wounds, by fracture or dislocation of the vertebrae, or by concus- 
sion without injury to the vertebrae. The spinal cord is found 
simply disintegrated, or there may be much hsemorrhage and the 
disintegrated nerve tissue be mixed with blood. If life continue, 
the nerve elements may degenerate ; Gluge^s corpuscles and free fat 
droplets may form ; blood pigments may be formed ; and when in- 
flammation supervenes more or less pus may be intermingled "with 
the degenerated detritus. There may be marked changes in the 
minute structure of the cord, without any change being evident to 
the naked eye. 

SECONDARY DEGENERATIONS IN THE SPINAL CORD. 

When nerve fibres of certain parts of the brain and of the spinal 
cord are divided or destroyed from any cause, that portion of them 
which becomes separated from its trophic centres degenerates. After 
a time — frequentl}" two to four weeks — tlie medullary sheath and 
axis cylinder disintegrate, becoming granular and fatty. These 
products of degeneration may be in part absorbed at once, or may 
collect in cells, forming the so-called compound granular corpuscles. 
After a still longer time — sometimes several months — the degene- 
rated areas become gray in color from the absorption of the de- 
generated myelin, harder, and somewhat shrunken. These changes 
are partly due to the formation of new connective tissue which takes 
the place of the degenerated nerve fibres. 

Since the affected portion of nerve tissue becomes gray or 
translucent after the myelin is broken down and absorbed, and the 
new connective tissue is formed, this is often called Gray Degene- 
ration ; or, as the degenerated areas are harder than normal, it is 
sometimes called Sclerosis. 

Xow, it is found that this secondary degeneration takes place in 
the direction in which the fibres conduct — in centripetal or sensory 
fibres, upward ; in centrifugal or motor fibres, downward. Thus, 
we have Descending Gray Degeneration {Descending Sclerosis), 
and Ascending Gray Degeneration {Ascending Sclerosis). 

Descending Gray Degeneration. — This change affects only the 
motor nerve fibres, and may reach but a short distance from the seat 
of lesion, or may extend for a long distance, depending upon whether 
the severed fibres run a short or long course before reaching their 
termination — i.e., passing into ganglionic centres. Lesions of the 
brain, such as embolic softenings and apoplectic clots, which destroy 
or interrupt any of the motor nerve fibres originating in the central 
convolutions, may be followed by gray degeneration of the portion 
of the fibres situated peripherally to the lesion. These fibres pass 
through the corona radiata, anterior portion of the internal capsule. 



THE SPINAL CORD. 321 

pes pedunculi, pons, and thence to the anterior pyramids, where 
most of them decussate and pass to the posterior part of the lateral 
columns of the opposite side. Thcjse which do not decussate form a 
narrow band at the inner part of the anterior columns of the same 
side, constituting the columns of Tiirck. These fibres which con- 
vey motor impulses from the brain to the cord form a system called 
the i^yramidal tract. There are also short motor fibres in the ante- 
rior columns, forming the so-called anterior root zones, which 
maintain communications between different portions of the gray 
matter. 

jSTow, a lesion in the brain or medulla, destroying the continuity 
of the motor nerve fibres of the pyramidal tract, will be followed by 
areas of gray degeneration in the posterior part of the lateral column 
of the opposite side, and in a narrow band near the anterior longitu- 
dinal fissure of the same side (see Fig. 158). A lesion below the 




Fig. 158.— Descending Gray Degeneration. 
Section of cord in cervical region, showing secondary degeneration from softening in pons 
which had existed for at least six months. A, column of Tiirck on same side as brain lesion : 
B, pyramidal tract on opposite side. 

medulla, involving the fibres of the pyramidal tract, will bo followed 
by degeneration of the fibres on the same side below the point of 
lesion. Lesions involving the fibres of the anterior root zones will 
be followed by degenerations which extend but a short distance, 
since these fibres soon communicate with tluMr centres in the gray 
matter. If a part only of the fibres in any of these regions are inter- 
rupted the amount of degeneration is jiroportionati^ly small. 

Ascending (h-dij Beijcneraliou. -Any lesion intin-ruptiiig the 
course of the sensory nerve fibn^s in llu* cord is followed by degene- 
ration of the central ends of the involved fibres and inereast^ oi cow- 
nective tissue about them. Tlu^se fibres anMU iKut situattnl in the 
})osterior columns and t\)rni eonnnunieations betweiMi ditVerent part> 
of the gray matter — posterior root zones — and luMieehave not great 
length. Other sensory fibres are grou})ed in a narrow baud near the 



322 



THE SPINAL CORD. 



posterior longitudinal fissure, forming the columns of GoII, while 
other sets, forming the so-called direct cerebellar tract and the 
columns of Gowers, are situated in the periphery of the lateral 
columns. 

A lesion of the cord invoh'ing the severance or destruction of 
these centripetal fibres will be followed by gray degeneration of the 
entire posterior columns, and the cerebellar tract, and the columns of 



/J^^^^ft^^^'^' '%- -'''-^'X^ ^A^J^'' \*^ - ■^\ /I 




Fig. 159.— Asce>t)es'g Gray Degeneration. 
Section of cord in cervical region, showing secondary degeneration from a tumor in the dorsal 
region of eighteen to twenty months" duration. A, columns of Goll ; B, pyramidal tract ; 
C, columns of Gowers (antero-lateral ascending tract). Drawn from a specimen prepared by Dr. 
Ira Tan Gieson . 

Gowers for a short distance above the lesion. The fibres of the pos- 
terior root zone being short, however, the degeneration -will, at a 
short distance above the lesion, become limited to the columns of 
Goll, the direct cerebellar tract, and the columns of Gowers in the 




Fig. 160.— Ascent)ing Gray Degeneration, 
A small portion from edge of degenerated region of cord shown in Fig. 159, more highly 
magnified. A, normal nerve fibres ; B, degenerated area. 

lateral columns (Fig. 159). The degeneration may be traced along 
the columns of Goll to the restif orm bodies, and in the cerebellar 
tract to the cerebellum. Lesions invohdng the entire thickness of 
the cord will produce bilateral degenerations. 

It should be borne in mind, in looking for these secondary lesions, 
that they are not developed until considerable time has elapsed since 
the development of the primary lesion, and that when small areas 



THE SPIXAL CORD. 



?j2:} 



are involved they are usually inconspicuous. In any event, the 
lesions are apt to be more evident to the naked eye in sijecimens 
hardened in chromic fluids than when fresh, and microscopical 
examination is often necessary for their recognition (Fig. IGOj. 

INFLAMMATION. 

Acute Myelitis. 

This lesion of the spinal cord, which is sometimes distinctly in- 
flammatory in character and sometimes of a degenerative nature, 
is usually confined to a comparatively limited longitudinal extent 
of the cord, and hence is sometimes called transverse 'myelitis. 
When the cord is removed and laid upon the table, if the lesion 
is marked, a flattening of the cord at its seat may be observed ; or 
on passing the finger gently along the organ the affected segment 




Fig. 161.— Degenerated Tissue from Acute Myelitis. 

will be found softer than the rest of the cord. On making a section 
through the diseased portion the nerve tissue may be white or red 
or yellowish or grayish; it may be quite firm, but is usually moro 
or less softened and sometimes almost diffluent.* 

Microscopical examination shows different a})pearances, depend- 
ing upon the stage of the infianimatory or (li\i;vnerative process. 
There n\ay be much blood, or, if the lesion has existed for some time, 
blood pig-ments ; also fragments of more or It^ss degenerated iiervi> 
fibres and cells (Fig. 101), myelin dropli^is, frei^ fat granules, and 
larger and smalUu- cells filled with fat graiuiK\s ((Jliig(^'s corpiiselesK 
pus cells, granular matter, neuroglia, cells, and sonu^tinics corpora 
amylacea. The various combinations of these eleinent:^ givo rise 

' Tt sliouUl bo nMnciubercil that a imH-haiiical in jury to thr coi\l in ivnun al, siuh 
ascrushini;- or bruisiiiii;, may ri'diu'c {\\c injuicHl portion to ji pulpv oonsistonco ami 
thus iM'oduce appoaraiu'os somoAvhat similar to those of si^mo forms of iiitUimmatorv 
softening. 



32-1: 



THE SPINAL CORD. 



to the different gross appearances which the diseased part presents. 
In earher stages of the lesion the blood vessels may be dilated, the 
nerve fibres and cells swollen ; or the walls of the blood vessels may 
be thickened or fatty. 

The lesion is apt to commence in the gray matter or at its edge, 
and then extend first laterally and afterward upward and down- 
ward. 

In a certain number of cases the degenerated material may be 
absorbed and a cicatrix or cyst formed. In the least extensive forms 
of the lesion there is apparently a regeneration of the nerve fibres 
and a restoration of the functions of the cord. 

Secondary gray degeneration, both ascending and descending. 









-^ 



Fig. 162.— Poliomyelitis anterior. 
Showing degenerated area in anterior cornua, with atrophy of gray matter. A, atrophic 
region CWeigerfs haematoxylin stain). Specimen prepared by Dr. Ira Van Gieson. 

may occur in this form of myelitis, varWng in extent according to 
the size of the primary lesion. 

Acute disseminated Myelitis runs a rapid course, and proves 
fatal in a short time. The inflammation involves nearly the whole 
length of the cord, but is more intense in some places than in others. 
The cord is swollen and congested, it is infiltrated ^yiih. pus cells, the 
connective-tissue framework is swollen, and the nerve elements are 
degenerated. 

Poliomyelitis anterior (Myelitis of the anterior horns). — This 
name is applied to a group of cases which are characterized by clini- 
cal symptoms indicating changes in the anterior gray cornua. The 
disease occurs both in children and in adults, and varies in the 



THE SPINAL CORD. 



326 



severity, acuteness, cind duration of its symptoms. In many cases 
there is complete recovery, and then we must suppose that the 
changes in the nervous tissue were not destructive in their charac- 
ter. In other cases the symptoms are more permanent, indicating a 
destructive lesion. From the autopsies so far recorded we learn 
that the lesion is most frequent at the lumbar and cervical enlarge 
ments of the cord, but may occur anywhere, and is often in scattered 
patches (Fig 102). There is degeneration, shrinkage, pigmentation, 
and atrophy of the ganglion cells in the anterior gray cornua (Fig. 163). 
There may be an increase of connective tissue in the gray cornua 
and in the anterior and lateral columns. There may be degenera- 
tion and destruction of a considerable part of the anterior cornua ; 







1 .-' 'i r '<- 1',' '?>2 : V. t - 






Fig. 163.— Poliomyelitis anterior. 
Showinpr portion of Fiff. 1^2 at edp:e of affected area, more hijjlily majrnifled. A. normal 
ganglion cells surrounded by nerve fibres ; B. degenerated ^angliou cells ; C, granular masses at 
place of ganglion cells ; D, small cavity containing fluid. 

tliere nuiy be atrophy of the anterior nerve roots. Tlio cord may be 
considerably distorted as the result of tlu^ lesion. 



CJiroific MjicJitis. 

Chronic Interstitial 3fi/cl if is. —JJndcv this heading are em- 
braced a variety of lesions wliicli probably ditV(M- from om^ another 
somewhat in the nature of tlie clKuip^s involviMl. but more in x\w 
seat of the disease. We sliall consiihM- without spoci.d elassitieatiou 
th(» most important forms. 

(Vu'onic TraHsrcrse Mi/cli/is.- liiiHM-tain ea>rs of pivssiuv on 
tlu^ spinal cord from a tumor or from displjuuMuent of the bones o( 
tlie V(M-tebral column, etc., instead of becoming softened or undergo- 



v)26 THE SPINAL CORD. 

ing acute inflammatory changes, the cord becomes the seat of a lo- 
cahzed formation of new connective tissue, with consecutive atrophy 
of more or less of the nerve elements in the gray and white matter. 
The cord becomes in this way harder, and sometimes shrunken at 
the seat of lesion, and grayish in color. This change inay be fol- 
lowed by ascending and descending gray degeneration. 

Multiple Sclerosis, — This lesion, similar in its nature to multi- 
ple sclerosis of the brain, and of ten occurring mth it, seems to belong, 
like other chronic inflammations of the cord considered in this section, 
to the group of chronic interstitial inflammations. It consists in the 
formation, in more or less numerous scattered, circumscribed areas, 
of new connective tissue, apparently derived from the neuroglia. 







"^v 








'^ , 



'^fiSfi^ 






^fnk^ 



/ 

V 




Fig. 164.— Posterior Spinal Sclerosis. Upper dorsal region. 

The formation of new connective tissue is accompanied by degene- 
ration and atrophy of the nerve fibres and ganglion cells. Whether 
the formation of new connective tissue is primary and the atrophy of 
the nerve elements secondary, or vice versa, it is difficult to say. 
The new connective tissue consists of the characteristic branching 
neuroglia cells, surrounded by a more or less dense network of fine 
fibrillse, many if not most of which seem to be branches of the neu- 
roglia cells. Corpora amylacea and sometimes fat droplets, either 
free or contained in cells, may be present in the sclerosed areas. 

The areas of sclerosis may involve both gray and white matter, 
and may be very small or large. If very small or in early stages of 
formation, they may not be recognizable by the naked eye, but when 
^^sible they are gra^dsh, translucent, and firmer than the surround- 



THE SPINAL CORD, 



327 



ing tissue, and may or may not present a depressed surface ; they 
sometimes project above the general level. The cause of this, as of 
other forms of so-called idiopathic interstitial myelitis, is very ob- 
scure. 

Posterior Spinal Sclerosis {Locomotor Ataxia). — This lesion 
consists essentially in a degeneration and atrophy of the nerve fibres 
and an increase of connective tissue in the posterior columns of the 
sjjinal cord (Fig. 164). Not infrequently the posterior portion of 
the lateral columns, the posterior roots and cornua, are also in- 
volved. Exceptionally a large part of the lateral columns is in- 
volved, and also the anterior cornua. The change usually commen- 
ces in that portion of the posterior columns bordering on the poste- 




'^:^.7^. 



Fig. 165.— Posterior Spinai, Sclerosis. 

A portion of sclerosed area shown in Fig. 164, more highly magnified, a, new-formed con- 
nective tissue; b, bloodvessels; c, nerve fibres; d, atrophied nerve fibres. 

rior cornua, but may involve, as above stated, the adjacent parts. It 
is usually most marked in the lower dorsal and lumbar regions. 
The sclerosis may extend upward to the restiform bodies, but in the 
cervical region it is apt to be confined largely to the columns of Goll, 
although there are exceptions to this. 

When the lesion is well developed the pia mater over the affected 
area is usually thickened and adherent to the cord. In its early 
stages there may be no change evident to the naked eye ; but when 
advanced the posterior columns may appear somewhat depressed, 
and grayish and firmer than the rest of the cord. The microscopical 
appearances vary, depending upon the stage and extent of the lesion. 
The walls of the blood vessels may be thickened : there is more or 
less new connective tissue consisting of neuroglia cells and very 



328 THE SPINAL CORD. 

numerous interlacing, delicate fibrils. There may be numerous cor- 
pora amylacea and fat granules, either free or collected in cells. The 
nerve fibres may be numerous, but separated more or less widely by 
the new connective tissue, or they may be very few in number and 
irregularly scattered through the new tissue (Fig. 165). The atro- 
phy may involve the fibres of the posterior nerve roots and cornua, 
and even the ganglion cells of the latter. 

• According to the recent researches of Lisauer,' the columns of 
Clarke in the dorsal region show in this disease a very constant and 
marked diminution in the number of delicate fibrils which under 
normal conditions surround the ganglion cells. 

In the rare cases in which the sclerosis extends to the lateral col- 
umns and to the anterior cornua, the minute characters of the le- 
sions are the same. 

There are other less important and less well understood forms of 
sclerosis of the white matter and degenerative or inflammatory 
changes in the gray matter of the cord ; but, so far as we know, the 
character of the lesions is essentially the same as those above de- 
scribed, except in their distribution. They are associated either ^yith. 
paralysis or changes in the muscles, and the secondary changes are 
for the most part better known than the primary alterations in the 
cord. Such lesions, which the scope of this book does not* permit us 
to enter into, are lateral sclerosis, peripheral sclerosis, the lesions 
involving muscular atrophy, etc. 

Solitary tubercles and gummata may occur in the spinal cord, 
but are not common. 

TUMORS. 

Cysts may occur as a result of softening or from unknown causes. 
Sometimes very long, narrow canals are found in the spinal cord, 
even reaching nearly its whole length. Some of these are evidently 
the dilated central canal, as they are lined with epithelium. Others, 
however, have been found behind the central canal, and their mode 
of origin is unknown. 

In the pia mater of the cord are sometimes found small fibro- 
mata, osteomata, and lipomata. 

Endotheliomata, of the same types as have been described as ex- 
isting in the pia mater of the brain, are much more rarely found in 
the pia mater of the cord. 

A fatty sarcoma "" of the pia mater which infiltrated the cord, 
formed a tumor as large as a filbert, and had for twelve years 
caused gradually increasing paraplegia, has been described. 

^ Fortscbritte der Medicin, Bd. ii., No. 4, 1884. 
'^ Trans. Lond. Path. Soc, xxxix. 



THE SPINAL CORD. 



3;>9 



Three curious cases ^ of diffuse sarcoma of the pia mater of the 
whole length of the cord are recorded. They occurred in girls of 
4:i, 16, and 22 years of age. In each case the pia mater of the whole 
length of the cord was diffusely thickened and studded with nodules. 
In two of the cases the growth was composed of round cells, in the 
third case of large endothelial cells arranged in alveoli. In two of 
the cases the clinical symptoms lasted only for about three weeks, in 
the third case for five months. The acuteness of the symptoms was 
such as to indicate the existence of spinal meningitis. 

In the spinal cord itself gliomata, fibromata, sarcomata, glio- 
sarcomata, and angio-sarcomata occur but rarely. 

When gliomata or glio-sarcomata do occur in the spinal cord, the 
new growth is apt to extend for some distance lengthwise in the 



— a 




Fig. 166.— Syringomyelia. 
Transverse section of cord. A, white substance of cord, distended by tumor; B, B. dis- 
torted and atrophied gray substance of anterior cornua; C, tumor mass (glio-sarcoma) ; D, 
cavity in cord. Drawn from specimen prepared by Dr. Van Gieson. 

cord and to be attended with the formation of a cavity ; this condi- 
tion is usually described under the name of syringomyelia. 



SYRINGOMYELIA. 

This lesion of the spinal cord consists in the formation of giio- 
matous or glio-sarcomatous tissue in the vicinity of the central 
canal, and its subsequent partial disintegration with the formation 
of one or more cavities within the substance of the cord (Fig. IGG). 
These cavities, which are filled with fluid, vary greatly in size, shape, 
and extent, and, while usually situated in the central region of the 
cord, they may involve the anterior and posterior cornua and invade 
the posterior columns. There may be two communicating cavities, 
and these may, but usually do not, open into the central canal. The 

^ Trans. Londou Path, Soc, xxxviii. Arch, fiir Psych., 1885. 
29 



330 THE SPIXAL CORD. 

longitudinal extent of these cavities varies greatly. The lower 
cer\dcal and upper dorsal regions are most frequently involved. The 
cavity is usually lined w4th tissue somewhat denser than that which 
makes up the bulk of the tumor. The gliomatous or glio-sarcomatous 
tissue which forms the basis of the lesion in syringomyelia probably 
originates from the layer of neuroglia which surrounds or extends 
away from the central canal. 

- Syringomyelia is frequently mistaken for hydromyelia (see below), 
which is a congenital malformation, and in which the longitudinal 
cavity in the cord is at some period lined ^^4th epithehal cells. 

There seems, furthermore, to be a class of lesions of the cord, 
usually classed as syringomyelia, in which caAT.ties of various forms 
co-exist with a tumor in the vicinity of the central canal. But these 
cavities do not appear to be formed by a breaking-down of the tumor 
tissue, but in some other way as yet little understood. 

MALFORMATIONS. 

The spinal cord may, in so-called monsters, be double either in 
circumscribed portions or over a large part of its extent. ^ It may be 
unusually long or short, or it may be absent altogether (amyelia). 
This usually occurs with anencephalia. Under these conditions a 
long connective-tissue sac, filled with more or less fluid, may occupy 
the spinal canal. 

Hydromyelia (Hydrorrhachis interna). — This abnormality con- 
sists in the dilatation of the central canal of the spinal cord by fluid 
(Fig. 167). This may be moderate, or so extreme that but little of 
the substance of the cord is left as a thin shell around the central 
cavity. When they have not been destroyed by atrophy, epithelial 
cells may be found lining the cavity. 

Hydrorrhachis externa. — In this lesion there is an accumulation 
of fluid between the meninges of the cord, causing more or less 
atrophy of the latter. 

Hydromyelocele — Spina bifida. — In the majority of cases 
hydrorrhachis is accompanied by a more or less complete lack of 
closure of the spinal canal posteriorly, so that the collections of fluid 
within may pouch outward through the opening in the form of a 
sac. The sac may be covered by skin, or this may be absent, either 
from the beginning or as a result of thinning and rupture. The 
walls of the sac may consist of the dura mater and pia mater, or, in 
cases of hydrorrhachis externa, of the dura mater alone ; when both 

^ According to Van Gieson, the apparent doublings of tlie spinal cord which have 
been frequently described in adults are due to bruises and injuries of the cord in- 
flicted, after death, during or subsequent to its removal from the body by instruments 
or by incautious handling. New York Medical Journal, 1892. 



THE SPINAL CORD. 



.331 



:are present they are usually more or less fused together. Inside of 
the membranes of the sac there may be a shell of distended nerve 
tissue of the cord ; or the spinal cord may be split posteriorly and the 
sides crowded sideways ; or there may be a rudimentary fragment of 
the cord suspended in the sac or attached to the walls ; or the cord 
may be but little changed and remain inside the spinal canal. The 
openings in the spinal, canal may be due to the complete or partial 
absence of the vertebral arches, or more rarely the sac may protrude 
through openings between the completely formed arches. Spina 
bifida most frequently occurs in the lumbar and sacral regions, but 
it may occur in the dorsal or cervical regions, or the canal may be 
open over its entire length. Very rarely it is open on the anterior 
surface. The protruding sac may be very small or as large as a 




i^••^■■>;-■■'aT-?•/^••i^^'o^^•■•'"':^■^■••ilv■-^\'^^,?•^V.^? . 





Fig. 167.— Hydromyelia. 

In the section from which this drawing was made, the epithehal cells surrounding the di- 
lated central canal were well preserved. 

chikVs head. The fluid in the sac is usually clear, but may be turbid 
from flocculi of degenerated nerve tissue. 

THE PERIPHERAL NERVES. 



CHANGES IN NERVES AFTER DIVISION. 

When nerves are divided or a portion destroyed by injury, the 
nutrition of certain parts of the fibres is interfered ^vith, apparently 
because of their separation from their trophic centres, and they suffer 
degeneration ; but after a time, if the conditions be favorable, thoy 
may undergo regeneration and restitution of function. The degene- 
ration not only affects the entire severed portion, but it occurs at 
nearly the same time in all parts. The degeneration consists in 
the breaking-up of the medullary sheaths into variously shaped 
vdroplets, and the decomposition of these, with the formation of fat, 



332 THE SPIXAL CORD. 

whicli may remain for some time either free or enclosed in cells, and 
finally be absorbed (see Fig. 168). The axis cylinder, too, is, in many 
cases at least, more or less completely destroyed. The neurilemma 
and its nuclei do not seem usually to undergo degeneration, but may 
persist and take part in the regeneration of the nerve when restitu- 
tion occurs. 

After a variable time, if the conditions are favorable, the divided 
ends of the nerve may be united, and a regeneration or new forma- 
tion of nerves in or about the severed portions may occur, so that the 
function may be resumed. Considerable tiane is required, frequently 
months, for the completion of the regenerative process. Degenera- 
tion of the nerves not only follows mechanical injuries, such as inci- 
sion, crushing or tearing, and compression, as from a tumor or dis- 
location of the bones, but it may result from disease of the special 
nerve centres with which the nerves communicate, or from inflam- 
mation of the nerves themselves. 

IXFLAMMATIOX. 

Acute Exudative yeuritis. — Primary acute inflammation of 




Fig. 168.— Degexeration of Nerve Fibres in Multiple Neuritis. 

From a case of alcohol poisoning. Specimen stained with osmic acid. The broicen-down 
medullary sheath and fat droplets are stained deep black. 

the nerves may occur as the result of injury, or it may be secondary 
to an inflammatory process in its vicinity, although, o^ving to the 
dense lamellar sheaths and the special blood supply, the nerve trunks 
may escape participation in even very severe inflammatory processes 
in surrounding tissues. The inflamed nerve may be red and swollen 
and infiltrated ^vith serum and pus cells. The j^rocess may undergo 
resolution or terminate in gangrene and destruction of the nerve, or 
it may become chronic and result in the formation of ne^v connective 
tissue. 

Degeneration and regeneration of the neri^e fibres, similar to 
those above described as following division of nerve trunks, may oc- 
cur in acute neuritis. 

Chronic Interstitial Neuritis. — This is essentially a chronic in- 
terstitial inflammation resulting in an increase of connective tissue in 
the nerve sheath and intrafascicular bands. As a result of this the 
nerve fibres undergo atrophy from pressure ; the medullary sheath, 
and finally the axis cylinder, being, in more or less of the fibres, par- 
tially or completely destroyed. 



THE SPINAL CORD. 333 

Multiple Neuritis. — Under a variety of conditions, such as ex- 
posure to cold and wet, overexertion, poisoning by alcohol, arsenic, 
lead, etc., and in connection with the acute infectious diseases, a de- 
generation of the nerve fibres in various parts of the body may occur 
(Fig. 168), Avhich may be accompanied with or followed by prolifera- 
tive changes in the neurilemma cells. Regeneration of the affected 
nerve fibres may occur -under these conditions, as after experimental 
division of the nerves, leading to their restitution. ^ In some forms 
of multiple neuritis the inflammation is exudative in character, and 
new cells of various forms are found within and between the nerve 
fibres. The exact part which the neurilemma and other intrafasci- 
cular cells play in the inflammatory and regenerative changes of 
nerves is not yet very fully made out. 

Syphilitic and Tubercular Inflammation of the nerves is not 
common except at their central ends, in connection with similar in- 
flammations of the meninges, or when they are secondarily involved 
in connection with these inflammations in neighboring tissues. 

Leprous Inflammation.— This consists in the formation within 
the nerve of masses of new- formed tissue somewhat resembling 
granulation tissue, in whose cells multitudes of characteristic bacilli 
are uniformly found (see Leprosy). It constitutes the variety of 
leprosy known as lepra ancesthetica. 

TUMORS. 

The tumors of the nerves are such as consist largely of or con- 
tain new-formed nerve tissue — true neuromata j and the so-called 
false neuromata (Figs. 133 and 124), which are for the most part 
fibromata or myxomata of the connective tissue of the nerve. 
Myxo-sarcomata are less common, and jjrimary sarcomata rare. 
The nerves may be secondarily involved in sarcomata or carcino- 
mata, though not infrequently nerves pass through these tumors 
without being in the least involved in their peculiar structure. Pal- 
tauf has recently described as endotheliomata rare tumors of the 
glandula carotica.^ 

METHODS OF PREPARATION OF NERVE TISSUE FOR MICROSCOPICAL 

STUDY. 

The general methods of hardening have already been given on pages 
10 and 18. For minute study there is no one method of staining and 
mounting upon which we can rely exclusively for the study of all 

'Cousiilt Starr, ''Multiple Neuritis." The Middletou Goldsmith Lecture for 
1887. Trans. New York Patholoo-icnl Society. 1887, p. 1. 

'^Paltauf, Zieglcr's Beitrilge zur path. Anatomic, etc., Bd. xi., p. '^OO. 1880. 



334 THE SPINAL CORD. 

lesions. A preliminary examination of areas of inflammatory soft- 
ening, or of the disintegrated tissue in apoplectic clots, or of the 
new-formed tissue in chronic hcemorrhagic pachymeningitis inter- 
na, may he madehj teasing portions of the affected tissues in one-half- 
per-cent salt solution. Or the tissues in these lesions, or in any others 
in which fatty degeneration is suspected, may be placed for twenty- 
four hours in one-per-cent aqueous solution of osmic acid, and then 
washed and teased in glycerin. In this way the myelin and the fat- 
will be stained brown or black. Secondary and other degenerations 
of medullated nerves may be studied by soaking the nerves for 
twenty-four hours in one-per-cent solution of osmic acid, and then 
staining with picro-carmin and teasing and mounting in glycerin. 
Suppurative inilammation of the central nervous system and its 
membranes, or the connective-tissue changes in general, may be 
studied in sections from the tissues hardened in Miiller's fluid and 
alcohol, stained double with hsematoxylin and eosin (see page 52), 
and mounted in Canada balsam. 

A very useful method of staining sections of nerve tissue, espe- 
cially of the brain and cord, is that known as Weigert's heematoxy- 
lin method. The tissue is first well hardened in Miiller's fluid. 

Blocks of the hardened tissue are embedded in celloidin and sec- 
tions made in the usual way. The sections are first soaked for 
twenty-four hours in a saturated aqueous solution of neutral cupric 
acetate diluted ^vith an equal bulk of water. They are now thoroughly 
washed twice in water, then in alcohol, and then are transferred to 
the hsematoxylin solution, made as follows : 

Hsematoxylin crystals 1 gm. 

Alcohol, 97 per cent 10 c.c. 

Water 90 '' 

Saturated aqueous solution Lithium Car- 
bonate 1 '^ 

In this solution the sections remain for two hours. (If the finer 
fibres of the cerebral cortex are to be brought out the sections must 
remain for twenty-four hours in the hsematoxylin solution. ) The 
sections are now thoroughly washed in two or three waters and 
transferred to the bleaching solution, composed as follows : 

Potassium Ferricyanid 2.5 gm. 

Sodium Biborate .... 2. " 

Water 200 c.c. 

In this fluid the sections discharge a brownish color, and they 
remain in it until the gray matter has a distinct yellow color and 



THE SPINAL CORD. 335 

the white matter is bluish-black. The time required to produce this 
effect varies considerably, but is usually from one-half an hour to 
an hour. The sections are now washed, dehydrated with alcohol, 
cleared up in oil of cloves or oil of origanum, and mounted in 
balsam. The sections may be stained in alum carmin before de- 
hydration, to bring out the nuclei. 

In sections stained by this method the gray matter, connective- 
tissue elements, and ganglion cells have a yellow or yellowish- 
brown color, the axis cylinders are uncolored or have a slight yel- 
lowish tint, while the medullary sheaths are bluish-black or black. 

To demonstrate the presence of miliary aneurisms in or about 
apoplectic clots, it is usually necessary to macerate the brain tissue in 
water until the nerve elements disintegrate, and they may then be 
washed away under a stream of water, leaving the blood vessels 
with their aneurisms exposed. 



THE EESPIEATORY SYSTEM. 



THE LARYNX AND TRACHEA. 



MALFORMATIONS. 



The IsiVjnx and trachea may be entu*ely absent in acephalic mon- 
sters. The larynx may be abnormall}" large or small. The epiglot- 
tis also may be too large or too small, or may be cleft. There may 
be communications between the trachea and the oesophagus, and then 
the pharynx generally ends in a cul-de-sac, and the oesophagus opens 
into the trachea. There may be imperfect closure of the original 
branchial arches, so that there are fissures in the skin leading into 
fistulse which open into the pharynx or trachea. The fissure in the 
skin is small and is situated about an inch above the sterno-clavicu- 
lar articulation, usually on one or both sides, more rarely in the mid- 
dle line. Individual cartilages, as the epiglottis, or one or more 
rings of the trachea, may be absent, or there may be supernumerary 
rings. The trachea may divide into three main bronchi instead of 
two, and in that case two bronchi are given off to the right lung 
and one to the left. The trachea may be on the left side of the 
CBSophagus or behind it. 

INFLAMMATION. 

Acute Catarrhal Laryngitis. — This occurs as an idiopathic in- 
flammation, as a complication of the exanthemata and the infectious 
diseases, and is produced by the inhalation of irritating vapors and 
of hot steam and smoke. The inflammation varies in its intensity in 
different cases. The mucous membrane is at first congested, swol- 
len, and dry ; then the mucous glands become more active and an 
increased quantity of mucus is produced. There is an increase in 
the desquamation of the superficial epithelial cells and in the pro- 
duction of the deep cells. A few pus cells are found in the mucus 
and in the stroma of the mucous membrane. For some reason in- 
flammation of the larynx is frequently attended ^vith spasm of its 



THE RESPIRATORY SYSTEM. 



337 



muscles, thus producing attacks of suffocation. In severe cases 
cBdema of the glottis may be developed. 

After death the congestion of the mucous membrane frequently 
disappears altogether. 

Chronic Catarrhal Laryngitis. — The surface of the mucous 
membrane is dry or coated with muco-pus. The epithelium is thick- 
ened in some places, thinned in others, or in places entirely destroyed. 
The stroma is somewhat infiltrated with cells, diffusely thickened, or 
forming little papillary hypertrophies, or thinned, or necrotic and 
ulcerated (Fig. 169). 

The mucous glands are swollen and prominent. The inflamma- 



•'■«.>!.'t, ("'■■S.'^'"'!.'.. 



,r ,,--^'^— '-^ 



/ 



X 








-o:J 






1 -^^ Vv^^^^l 

f , J.T-j^^-'-' '.' '/• --a 

Fig. 1G9.— An Ulcer of the Larynx in Chronic Catarrhal Laryngitis, x 850 and reduced. 

tion may extend to the perichondrium of the cartilages and thus 
cause their necrosis. The most severe forms of chronic larvno'itis are 
those associated with pulmonary phthisis. Some forms of chronic 
laryngitis with thickening of epithelial and submucous tissue are 
called Pachydermia laryngis. 

Acute Suppurative Inflammation may attack the posterior sur- 
face of the epiglottis and the aryepiglottidean ligaments. The 
stroma of the mucous membrane is swollen and infiltrated with 
serum and pus. Abscesses may be formed in the stroma, which 
rupture internally, or extend outward into the neck, or into the wall 
of the })liarynx or of the a^sophagus. Suppurative intlamniatiou 
may accompany catarrhal, croupous, tubercular, and syphilitic laryn- 



338 



THE RESPIRATORY SYSTEM. 



gitis, inflammations and injuries of the pharynx and tonsils ; it may^ 
compHcate typhoid fever and the other infectious diseases. 

Croupous Laryngitis occurs most frequently as one of the le- 
sions of diphtheria ; it complicates the exanthemata and the infec- 
tious diseases. It is produced by the Bacillus diphtherige, by strep- 
tococci, by the inhalation of irritating gases, hot steam or smoke, 
and by the introduction of foreign bodies. 

• The mucous membrane is swollen and congested. Its surface is 
coated with fibrin and pus, and its stroma is infiltrated with fibrin 
and pus. The epithelial cells undergo coagulation necrosis. It is 
not often that there is necrosis of the deeper tissues. 



'r-t. 



<rf3'C) <-" J 



> t>-^ ?^^2:i_-«^>L«J^^'C 



4* ij 



:^if'r. 

















JV «~v^ 



l-«r_o«, 



'4 ^-^fZ 









^ ^ 

^:! 






oaf 







Fig. 170.— Tubercular Laryngitis. 



Syphilitic Laryngitis. — Syphilis often causes laryngitis. The 
inflammation may have the ordinary characters of an acute or 
chronic catarrhal inflammation, or it is a productive inflammation 
with the formation of new tissue in the stroma of the mucous mem- 
brane. This new tissue is principally composed of small cells, which 
often degenerate and die. In this way the mucous membrane of the 
larynx and the tissues beneath are thickened in some places and de- 
stroyed in others, these changes being especially marked in the upper 
portion of the larynx. If the perichondrium is involved by these 
changes there may be necrosis of the laryngeal cartilages. 

Tubercular Laryngitis in its simplest form consists of a catarrhal 
inflammation, a growth of new cells in the stroma, and the forma- 



THE RESPIRATORY SYSTEM. 33'.)* 

tion of tubercle granula in the stroma without necrosis. The mu- 
cous membrane is thickened ; it is coated with a layer of mucus, 
pus, and desquamated epithelium. From the epithelial la^^er out- 
ward the stroma is infiltrated with cells and with tubercle granula 
(Fig. 170). 

When there are added to the production of tubercle tissue an ex- 
cessive formation of cells and a tendency to necrosis, the conditions 
become much more serious and complicated. The catarrhal infiam- 
ination is intense, with the production of large quantities of pus and 
mucus. The necrosis results in the formation of ulcers of different 
sizes and shapes ; the inflammation and necrosis extend from the 
mucous membrane to the wall of the larynx. The epiglottis, the 
vocal cords, and the adjacent mucous membrane are coated with 
muco-pus ; their surfaces are ragged and irregular. In places the 
mucous membrane is destroyed, so that ulcers are formed ; in places 
it is thickened and infiltrated with cells and tubercular tissue ; in 
places it is necrotic. In the most severe cases the entire thickness of 
the wall of the larynx, with its cartilages, is involved. 

(Edema of the Glottis is the name given to serous infiltrations 
of the mucous membrane of the upper part of the larynx. The 
swelling is most marked on the posterior wall of the epiglottis, in 
the aryepiglottidean ligaments and the false vocal cords. In these 
places the oedema of the stroma of the mucous membrane may be 
sufficient to close the larynx. 

Acute oedema is due to an inflammatory exudation of serum, and 
accompanies inflammations of the pharynx, larynx, and neck. 

Chronic oedema is of dropsical character and is caused by disease 
of the heart, pulmonary emphysema, and compression of the veins, 
of the neck. 

TUMORS. 

Retention cysts of the mucous glands of the larynx may reach, 
such a size as to form sacs projecting into its cavity. 

Papilloma is the most frequent form of tumor of the larynx. 
The tumors grow most frequently from the vocal cords. They con- 
sist of a connective-tissue stroma arranged so as to form papilliB 
covered, with, epithelium. They are sometimes congenital. 

FibroDiata, lipomata, myxomata, and angiomata are occa- 
sionally met with. 

Chondroniata grow from the normal cartilages and are usually 
multiple and sessile. They may project into the cavity of the larynx. 

Sarcomata of the larynx have been seen in a considerable num- 
ber of cases. They occur both in children and in adults. They are 
composed of fusiform or round cells, with a' stroma which varies in 
quantity in the different cases. 



."340 THE RESPIRATORY SYSTEM. 

Carcinomata may invade the larynx from the tongue or the 
pharynx, or may originate in it. They are composed of flat epithehal 
cells packed together in the usual way. 

In the trachea tumors are of rare occurrence, but occasional 
examples of growths similar to those in the larynx have been met 
with. 

Cheesy and otherwise altered bronchial lymph nodes may by ul- 
'Cerative processes enter and obstruct the trachea. 

THE PLEURA. 
HYDROTHORAX. 

Non-inflammatory accumulations of clear serum in the pleural 
cavities are of frequent occurrence. They are produced by the 
same causes which effect dropsy in other parts of the body — le- 
sions of the heart, liver, and kidneys, and changes in the circulation 
and in the composition of the blood. 

If the amount of serum is small it is of little consequence ; if it 
is large it may compress the lower lobes of the lungs and interfere 
with respiration. 

There may be changes in the endothelium of the parietal pleura. 
Instead of the regular endothelium, large and small flat cells of ir- 
regular shape are found. 

HEMORRHAGE. 

Extravasations of blood in the substance of the pleura are found 
in persons who have died after suffering from the infectious dis- 
eases ; and as the result of injuries to the wall of the thorax. 

Blood in large quantity in the pleural cavities is found after rup- 
ture of an aneurism of the heart with rupture of the pericardium. 

Bloody serum in the pleural cavities is not often found with ordi- 
nary pleurisy. But with tubercular pleurisy and traumatic pleurisy 
it is not infrequently present. 

INFLAMMATION. 

The inflammations of the pleura are all spoken of by the common 
name of pleurisy, or pleuritis. 

All the different inflammations of the lung are capable of being 
accompanied by pleurisies, which begin in the pulmonary pleura 
^nd extend to the costal. 

Besides these, however, there are many pleurisies which belong 
primarily to the costal pleura and extend from there to the pulmo- 
nary pleura. 

Such pleurisies occur as idiopathic inflammations, as complica- 



THE RESPIRATORY SYSTEM. 341 

tions of various diseases, as the result of injuries^ or are j>ro(luce(l by 
the inflammation of adjacent parts. 

We can distinguish : 

I. Pleurisy with the production of fibrin. 
II. Pleurisy with the production of fibrin and serum. 

III. Pleurisy with the production of fibrin, serum, and pus. 

TV. Chronic pleurisy with the formation of adhesions. 
Y. Tubercular pleurisy. 

All the varieties of pleurisy can best be studied in the lesions, 
which are developed in and on the costal pleura. The lesions can be 
observed in the human subject, and can be produced artificially in the 
lower animals. It is in these artificial pleurisies especially that we 
are able to see the early changes produced by the inflammation and 
to watch the process step by step. 

The free surface of the costal pleura is covered with a single layer 
of flat cells — the endothelium. The pleura itself is formed of planes 
of connective tissue reinforced by elastic fibres. Connective-tissue 
cells with large bodies and branching processes are present in con- 
siderable numbers, being most abundant in the layers beneath the 
endothelium. In the connective tissue are embedded blood vessels, 
lymphatics, and nerves. 

I. Pleurisy with the Production of Fibrin — Dry Pleurisy — 

Acute Pleurisy. 

This form of pleurisy is apt to involve circumscribed areas of the 
costal, mediastinal, diaphragmatic, or pulmonary pleura, less fre- 
quently the entire pleura of one side of the chest. While the 
inflammation is going on the affected portion of pleura is coated 
with fibrin, the surface of the opposite portion of pleura is coated in 
the same way, and bands of fibrin join the two together. After the 
inflammation has run its course we find the affected portion of pleura 
thickened by the formation of new connective tissue, while bands of 
connective tissue extend between the opposed pleural surfaces. 

As an exceptional condition there is inflammation of the entire 
pleura of one side, with the production of such an enormous amount 
of fibrin as to compress the lung and cause death. 

II. Pleurisy with the Production of Fibrin and Serum — Pleurisy 

tvith Effusion — Subacute Pleurisy. 

This is the most common form of pleurisy. As a rule, it involves 
the greater part of the pleura of one side of the chest. Sometimes, 
however, tlie pleura of both sides of the chest is involved, and then 
the pericardium also is often inflamed. 



34-^ THE EESPIRATORY SYSTEIM. 

AVhile the inflammation is in progress the surface of the affected 
-pleura is coated Trith nbrin. and bands of fibiin stretch between the 
parietal and pulmonary plem'a. In the pleiu^al cavity is serum in 
variable quantity. This serum is clear, or turbid from the presence 
of pus cells and flocculi of fibrin. The lung is compressed in different 
degrees and positions, according to the quantity of the seriun and 
xhe character of the adhesions. 

If the patient recover the serum is absorbed, the fibrin disappears, 
and there are left behind connective-tissue thicke ni ngs of the pleura 
and adhesions. 

These tw.j forms of pleurisy, although different in their clinical 
Tiistories, are vet anatomicallv essentiallv the sa.me. In both of 
them we find a regular sequence of changes. First, the production 
of fibrin and a few j^us cells, either with or without serum. Second, 
a gradual absorption of the serum and fibrin. Lastly, the formation 
of permanent new connective tissue in the form of adhesions or of 
thickenings of the pleura. Throughout the whole process the tissue 
of the pleura is but httle changed ; the products of inflammation, 
although they originate in the tissue of the pleura, do not infiltrate 
it. but make their way to its stu-face, there accumulate, and there 
undergo their different changes. Variations from the regidar course 
of the inflammation are effected by the excessive formation either of 
the fibrin, the pus, or the serum, and by the manner in which these 
inflammatory products are absorbed. 

If Tre endeavor to follow out the successive changes by Trhich the 
flbrin, pus. and serum make their appearance and then disapj^ear, 
and the way in which permanent ne^w connective tissue takes their 
j^lace, we encoimter several difficidties. It is difficidt to obtain 
autopsies which will give the lesions belonging to each successive 
day of the disease : the pleiu'a does not really show well if the pa- 
tient has been dead more than tvro or three hours before the autopsy; 
and in most cases the inflammation is too intense, its products are 
too abiuidant, to be easily studied. 

To ob^-iate these difiiculties we must resort to experiments on the 
lower animals. By injecting a solution of chlorid of zinc into the 
23leural ca^-ities of dogs we can excite pleurisies closely resembhng 
those which "we see in the human subject. By varying the amoimt 
of fluid injected we can obtain pleurisies of different degrees of 
intensitv. Bv usins; a niunber of animals ^ve can observe the course 
of the inflammation from hour to hour and from day to day. 

In such an artificial pleurisy the first change is congestion. The 
pleura is of a tmif orm bright-red color, its surface moist and shining. 
There is as yet no serum and no fibrin. Ah^eady, however, the en- 
dothehal cells have fallen oft' in patches, the superficial connective- 



THE RESPIRATORY SYSTEM. 



343 



tissue cells are swollen and increased in number, and a feAY x^us 
cells are present. These are all the changes for from half an hour to 
,six hours after the irritant has been applied to the pleura. 

The next step in the inflammatory process is the production of 
serum and fibrin. The serum collects in the bottom of the pleural 
cavity, the fibrin coats the pleura. As the fibrin is produced the 
pleura loses its natural moist and shining appearance. The fibrin 
appears first in the form of little granules, knobs, and threads be- 
tween the edges of the endothelial cells and overlying them. A few 
pus cells are entangled in the fibrin and infiltrated in the superficial 
layers of the pleura. The swelling and new growth of the connec- 




FiG. 171.— An Artificiaxi Pleurisy in ths Dog, of Twenty-four Hours' Duration, x 750 
■and reduced. 

Swelling and growth of connective-tissue cells in the pleura. 

tive-tissue cells are now well marked. The bodies of the branching 
cells are swollen, and small polygonal, nucleated cells, arranged in 
rows between the fibres of the basement substance, make their ap- 
pearance. By the end of twenty-four hours these changes are fully 
developed (Fig. 171). 

After this the production of fibrin, serum, and new connective- 
tissue cells continues, and by the third or fourth day the new connec- 
tive-tissue cells are present, not only in the superficial layers of the 
pleura, but also in the laj^er of fibrin coating its surface and forming 
.adhesions. 

By the fourth or fifth day the cells in the libriii are still more 



344 



THE RESPIRATORY SYSTEM. 



numerous ; blood vessels make their appearance, which can be in- 
jected from the arteries of the pleura (Fig. 172). 

After this the serum is gradually absorbed. The layer of fibrin 
and cells on the surface of the pleura exhibits a constant decrease of 
fibrin and increase of cells, and becomes more intimately connected 
with the surface of the pleura. 

By the fourteenth day the fibrin has disappeared and a basement 




Fig. 172. — Artificial Pleurisy in the Dog on the Fifth Day, x 750 and reduced. 
The layer of new tissue on the surface of the pleura. 

substance has been formed between the cells. Of the new cells the 
superficial ones are changed into endothelium, the deeper ones into 
branching cells. The changes in the adhesions between the pulmo- 
nary and costal pleura are the same as those in the layer of fibrin 
coating the costal pleura. 

The lesions of human pleurisy seem to be essentially the same as 
those of the artificial pleurisy just described. But the inflammatory 



THE RESPIRATORY SYSTEM. 345 

products are formed in larger quantities, a much longer time is re- 
({uired for their absorption, and the formation of new connective 
tissue follows more slowly. 

In these forms of pleurisy, therefore, two distinct processes take 
place : 

1. The blood vessels are congested, and through their walls trans- 
ude the plasma of the blood and a few white blood globules. 

2. The superficial connective-tissue cells are increased in size and 
number. 

The products of the first of these processes, the fibrin and serum, 
are regularly reabsorbed. 

The product of the second of these processes, the new connective- 
tissue cells, regularly increases until a layer of new connective tissue 
is formed. 

The natural termination of such a pleurisy is the recovery of the 
patient, with thickenings of the pleura and adhesions. 

The irregular terminations are : The death of the patient, the 
protracted existence of the fibrin and serum, and the change of the 
character of the inflammation so that pus is produced. 

Ill, Pleurisy with the Production of Fibrin, Serum, and Pus — 

Empyema, 

This form of pleurisy may occur under several different condi- 
tions. 

lo The inflammation is at the very outset of severe character, 
with the formation of pus. 

2. A pleurisy with the production of fibrin and serum, either 
gradually or suddenly, changes its character and pus is formed. 

3. Phthisical areas of softening, or abscesses of the lung, abscesses 
in the wall of the thorax, or in the liver, or in the abdomen, rupture 
into a pleural cavity and set up an empyema. 

•4. The inflammation may be not only purulent but also gangre- 
nous in character. The fluid in the pleural cavity, the fibrin and 
pus coating the pleura, and the pleura itself, may putrefy, with the 
proliferation of bacteria and the evolution of gases. This may take 
place either in a closed pleura or in one which has been opened. 

5. If there is an opening into a pleural cavity, either through the 
lung or through the wall of the thorax, there is air in the pleural 
cavity, in addition to the inflammatory products. Such a condition 
is called pf/o-pneumothorax. 

In all these different cases the pleural cavity is partly or com- 
pletely filled with purulent fluid, and the lung is either compressed 
against the vertebral column or partly adherent to the chest wall. 
Sometimes, however, the purulent fluid is shut in by adhesions, 
30 



346 THE RESPIRATORY SYSTEM. 

either between parts of the lung and the thoracic wall, or between 
the lung and the diaphragm, or between the lung and the pericar- 
dium, or between the lobes of the lung. 

The fluid in the pleural cavity is usually a thin, purulent serum, 
composed of serum, pus globules, endothelial cells, and pieces of 
fibrin. But sometimes this fluid is very thick and viscid. 

In empyema in its earlier stages the lesions are the same as 
those in pleurisy ^^dth effusion, mth the addition of pus in the serum, 
the fibrin, and the superficial layers of the pleura. 

In the inflammatory products are regularly found either strepto- 
cocci, or the pneumococcus of Frankel, or Staphylococcus pyogenes, 
or these species in various associations. 

In children the inflammation may remain in this condition for a 
long time, but in adiflts other changes in the pleura are soon devel- 
oped. 

These changes consist in the growth of a large number of small 
polygonal and round cells, the basement substance is split up, and 
the pleura is changed into a tissue resembling granulation tissue. 

The pleura is thus considerably thickened. Its surface is coated 
with fibrin and pus, or is bare like the surface of an ulcer. 

In this condition the pleura may remain for months or years, 
its inner layers formed of granulation tissue, its outer layers of dense 
connective tissue. 

Sometimes the cell growth is more active, necrotic changes are 
added, and so there is a conversion of portions of the pleura into 
pus. Such a suppuration may extend from the pleura to the fas- 
ciae, the muscles, the skin, the diaphragm, or the lungs. Thus the 
pus may find an exit, through the wall of the thorax, into the peri- 
toneal cavity or into the lungs. 

If the empyema becomes gangrenous the pleural ca\"ity contains 
foul gases, the purulent serum is dirty and stinking and swarms ^vith 
bacteria. The fibrin coating the pleura is of green or brown color. 
Portions of the pleura itself may also become gangrenous. 

In old cases the thickening of the pleura may reach an enormous 
degree and it may become calcified. ' The perichondrium of the car- 
tilages and the periosteum of the ribs may become inflamed, with ne- 
crosis of the cartilages and ribs or a production of new bone. 

Empyema is, therefore, a very much more serious lesion than 
the two forms of pleurisy just described. The lesions involve not 
merely the surface of the pleura, but its entire thickness. When the 



^ For a resume of our knowledge of various calcifications in the lungs, and allied 
conditions often called " lung stones," consult Poulalion, "LesPierres du Ppumon,'' 
etc., Paris, 1891 ; or Legry, Arch, gen.de Med., Mrach and April, 1892. 



THE RESPIRATORY SYSTEM. 34T 

pleura has thus been converted mto granulation tissue it is hardly 
possible for it to return to a normal condition. 

It is important to remember that in children the changes in the 
pleura itself are less profound, and that in adults they become more 
and more marked, according to the duration of the disease. 

IV. Chronic Pleurisy tvith the Formation of Adhesions. 

This form of pleurisy may follow one of the varieties of pleurisy 
just described, it may be associated with emphysema and chronic 
phthisis, or it may occur by itself. 

After death the pulmonary and costal pleura are found thickened 
and joined together by numerous adhesions. These changes may 
involve only a part or the whole of the pleura on one or both sides 
of the chest. 

The thickened pleura is covered with endothelial cells, which are 
increased in size and number ; the connective-tissue cells in the 
pleura are also increased in number, and the blood vessels are more 
numerous. 

The adhesions are formed of connective tissue resembling that of 
the costal pleura, containing blood vessels and covered with endo- 
thelium. 

V. Tubercular Pleurisy. 

In acute general tuberculosis miliary tubercles are often present 
in the pleura. In acute and chronic phthisis, besides the fibrin, pus, 
serum, and new connective tissue so often produced, there may also 
be miliary tubercles or larger, flat, cheesy nodules. 

There are, however, cases of tubercular pleurisy which have the 
characters of a local tubercular inflammation. Tubercles are either 
absent altogether from the rest of the body or of secondary import- 
ance to the pleurisy. 

This form of pleurisy involves the pleura of one side of the tiio- 
rax only. It may be rapidly developed, the patient dying at the end 
of two weeks ; or it may continue for months. It seems to be very 
fatal. 

The inflammation may be confined to the costal pleura or may in- 
volve also the diaphragmatic and pulmonary pleura. The gross a[)- 
pearance of the lesion varies. 

1. The pleura is thickened, its surface is bare of fibrin ; it is of a 
bright-red color from the congestion of the blood vessels, and this red 
surface is mottled with white dots — the miliary tubercles. In the 
pleural cavity is bloody serum. 

2o The pleura is thickened , it is thickly coated with fibrin : no 
tubercles are visible to the naked eye ; the pleural cavity contains 
clear serum. 






THE RESPIRATORY SYSTEM. 



3. The pleura is thickened and the pleural ca^-ity contains puru- 
lent serum. 

In all the cases the changes in the pleura itself are essentially the 
same. The thickened pleura is infiltrated ^^-ith new connective-tissue 
cells. Scattered through its entire thickness are tubercle granula. 
either single or joined together by diffuse tubercle tissue (Fig. 173). 
The smaller blood vessels show a grovvth of their endothelial cells. 




^ ^' .%;f^0W^^^^t^fe^^S^^S5^'- \ 







Fig. 173.— Tubercular Pleurisy, x 90 and reduced. 
Drawn from a vertical section of the costal pleura. 

TUMORS. 

Fibroma. — Little white or pigmented fibromata, of the size of a 
pin's head and scarcely raised above the surface, are often present in 
the pulmonary pleura. 

Larger fibrous tumors are formed in the deeper layers of the cos- 
tal pleura, and project into the pleural ca^^ity. They may become de- 
tached and are then found loose in the pleural ca^^ity (Lebert). 



THE RESPIRATORY SYSTEM. 349 

Lipoma. — Fatty tumors are formed Ijeneatli the costal pleura 
and project into the pleural cavity (Lebert). 

Carcinomata, sarcomata, and lymphomata are usually second- 
ary to similar tumors in other parts of the bod3\ 

A peculiar form of primary new growth in the pleura has been 
described by several observers. ^ It is associated with a pleurisy with 
the production of fibrin and serum. There is a diffuse thickening of 
the costal pleura, or circumscribed nodules of different sizes. 

The new growth seems to begin in the lymphatics of the pleura, 
which are distended with flat, nucleated cells. 

I (Delafield) have seen two of these cases. The first case was a 
woman, fifty-three years old, who was ill, with the symptoms of 
pleurisy with effusion, for four months. After death the left pleural 
cavity was found to be full of bloody, purulent serum. The costal 
pleura was moderately thickened and coated with a layer of fibrin 
and pus. Beneath the fibrin and pus was a thin layer of granula- 
tion tissue. In this tissue and in the pleura were anastomosing tu- 
bules filled with flat, nucleated cells. The tubules looked like lym- 
phatics. 

The second case was a man, sixty-three years old, who had s}inp- 
toms of pleurisy with effusion, for four months. After death the 
right pleural cavity was found half -full of bloodj^ serum. The cos- 
tal, diaphragmatic, and j)ulmonary pleura were coated with fibrin 
and contained numerous white nodules, some of them as large as a 
pigeon's egg. These nod ales were formed of a connective-tissue 
stroma enclosing irregular spaces and tubules filled with flat, nu- 
cleated cells. 

It is very difficult to class these tumors ; whether to call them by 
the name of carcinoma, sarcoma, or endothelioma it is not easv to 
say. 

THE BRONCHI. 
INFLAMMATION. 

Acute Catarrhal Bronchitis is a disease of \evy common occur- 
rence, but one which seldom proves fatal. Our knowledge of its 
lesions is derived from severe cases, from experiments on animals, 
from cases which are complicated by other diseases, and from the 
symptoms which we observe during life. 

The inflammation involves regularly- the trachea and the larger 
and medium-sized bronchi, less frequently the smaller bronchi also. 
As a rule, the bronchi in both lungs are ecpially aft'ected. 

^ BiniJi-TIirschfeld, "Path. Anat.," p. 76S. E. Wagmr, Arch d. Iloilkumio. xi. 
11. SchuU Arch, d llcillamdc, xv. Thicrfddcr, " Ml. d. path. Hist.. '•4 I.iet. 
Ffdnkd, Berliner kliu.. Wocheuschrift, ]\ lay 23d, 1S9'2. 



350 



THE RESPIRATORY SYSTEM. 



The first change seems to consist in a congestion and swelHng of 
the mucous membrane, with an arrest of the functions of the mucous 
glands. This is attended with pain over the chest, a feehng of op- 
pression, sometimes spasmodic dyspnoea, and a dry cough. After 
this the mucous glands resume their functions with increased activity, 
the congestion diminishes, there is an increased desquamation of epi- 
thelium, an increased formation of the deeper epithelial cells, and a 
moderate emigration of white blood cells. Sometimes the red blood 
cells also escape from the vessels. The patient now has less pain and 
oppression ; the cough is accompanied with an expectoration of mu- 
cus mixed with epithelium, pus, and sometimes blood. 








j\ ^ 



f iii 



W rTWTT-TB-ifrf 'l-ggfiS ai 



"-n-^Tin ■ faii wi ^ ii fa , 




Fig. 174.— Acute Catarrhal Bronchitis, x 850 and reduced. 

After death the only lesions visible are the increased amount of 
mucus, the growth of new epithelium, mucous degeneration of the 
epithelial cells, a few pus cells infiltrating the stroma, and the gene- 
ral congestion of the mucous membrane. The whole process is a 
superficial one, not producing any changes in the walls of the bron- 
chi beneath the mucous membrane (Fig. 174). 

When the inflammation involves the smaller bronchi also they 
may be full of pus, but their walls are unchanged. 

The filling of the small bronchi may result in the collapse of the 
groups of air vesicles to which they lead, and thus are produced areas 
of atelectasis;, which may be further changed by inflammatory pro- 
cesses. 



THE RESPIRATORY SYSTEM. 351 

Chronic Catarrhal Bronchitis,— Th\^ form of bronchitis may 
be the sequel of one or more attacks of acute bronchitis. More fre- 
quently it is associated with emphysema, heart disease, interstitial 
pneumonia, phthisis, pleuritic adhesions, or the inhalation of irritat- 
ing substances. 

There is in most cases a constant production of mucus, pus, and 
serum in considerable quantities, and these inflammatory products 
may have a very foul odor. Less frequently these products are very 
scanty — dry catarrh. 

In examining the bronchi in these cases after death we are often 
struck by the want of proportion between the symptoms and the 
lesions. The same bronchi which during life were constantly pro- 
ducing large quantities of inflammatory products and injuring the 
patient^s health, after death may be but little changed from the nor- 
mal. In other cases, however, the lesions are more marked. 

The bronchi contain mucus and pus ; they may be congested ; 
their walls are often trabeculated. The epithelium is deformed and 
desquamating, with a production of new cells in the deeper layers. 
The mucous glands are enlarged or atrophied. The connective-tissue 
stroma is thickened and infiltrated with cells. The coats of the ar- 
teries in the walls of the bronchi may be thickened. There may be 
cylindrical dilatation of one or more bronchi. The muscular coat 
may be thickened or thinned. Very frequently the epithelial cells 
of the air vesicles and air passages are increased in size and number. 
Acute Croupous Bronchitis occurs as a lesion of diphtheria, as 
associated with croupouis laryngitis, as the result of the inhalation of 
hot steam, with lobar pneumonia, and sometimes as an idiopathic 
disease. 

The bronchi are lined or filled with a mass of fibrin, pus, and de- 
squamated epithelium. Fibrin and pus may also be found beneath 
the epithelium and infiltrated in the stroma. 

Chronic Croupous Bronchitis is attended Avitli the formation in 
one or more bronchi of masses of fibrin w^hich are expectorated bv 
the patient in the form of branching casts of the bronchi. The dis- 
ease is a very chronic one, and is often associated with phthisis. 
After death the bronchi are said to be found but little altered from 
the normal, 

Curschmann ' has described under the name of "bronchiolitis 
exudativa " a form of bronchitis in which small threads and bands of 
gray or yellow, partly transparent, coagulated matter are formed in 
the small bronchi. Vierordt ' has found similar formations in lobar 

' Deutsch. Arch. f. klin. Med., xxxii. 

2 Bed. kliu. AVocheuscli., 1883. B. Levi, Zeitscli. f. kliu. ]\[ed.. ix. li>/dcn. 
Vircli. Arch., Bd. Ixxiv. 



o 



52 THE RESPIRATORY SYSTEM. 



pneumonia. Leyden and Levi have found them in broncno-pneu- 
monia. 

In different forms of bronchitis, especially in those associated 
with asthma, the exudation may contain small, octahedral bodies, 
probably composed of mucin. They are accidental formations, prob- 
ably formed from cells, and may be found in the sputa. 

/ 

BRONCHIECTASIA. 

Dilatation of the bronchi presents itself under three forms : the 
cylindrical, the fusiform, and the sacculated. 



r^ 



r^.(^-i'^ 






l- 



I 

If' 



I, 









Fig. 175.— Section of the Wall of a Bronchiectasia, x 850 and reduced. 

The cyhndrical dilatation is a uniform enlargement of one or more 
bronchi for a considerable part of their length. It is found in 
bronchi of every size, but most frequently in the medium-sized. 

The fusiform dilatation is a mere variety of the cyhndrical. The 
bronchus is uniformly dilated for a short distance, and then resumes 
its natural size. Several such dilatations may be found in the same 
bronchus. 

The sacculated dilatations form the largest cavities. These cavi- 
ties communicate with one side of the bronchus ; the peripheral por- 
tion of the bronchus may be obliterated. The bronchus leading to 
the cavity may be of normal size, or dilated, or stenosed, or even 



THE RESPIRATOKY SYSTEM. 3o3 

completely obliterated. Such sacculated dilatations may reach a 
very large size and may communicate with each other. 

Any inflammatory process which involves the thickness of the 
wall of a bronchus seems to be capable of producing dilatation of that 
bronchus. 

In acute general bronchitis and broncho-pneumonia in children, 
cylindrical dilatation of a number of the medium-sized bronchi is 
often produced. 

In the persistent broncho-pneumonia of children such dilatations 
reach a still greater development. 

In acute and chronic phthisis tubercular inflammation gives rise 
to sacculated dilatations, which expand with time and are made 
still larger by the destruction of the adjacent lung tissue. 

Chronic bronchitis may lead to cylindrical or sacculated dilata- 
tions, sometimes of great size. 

Occlusion of some of the bronchi, consolidation of portions of the 
lung, and extensive pleuritic adhesions, may also produce bronchi- 
ectasia. 

The walls of these dilatations may preserve the characters of the 
wall of the bronchus, more or less altered by inflammation (Fig. 
175), or these characters may be altogether lost. The dilatations 
may contain mucus and pus, or they may be empty. 

TUMORS. 

Ossification of the walls of the bronchi is sometimes found. 

Lipoma in the submucous connective tissue has been described 
by Rokitansky. 

Carcinoma of the walls of the bronchi may occur as a secondary 
lesion, but as a primary growth it is rare. It may be formed in the 
large or small bronchi, follow the course of the bronchial tree, or ex- 
tend to the lung tissue or to the trachea. 

Langhans describes a primary carcinoma of the lower end of 
the trachea and the large bronchi in a man fortv vears old. The 
lower end of the trachea and the large bronchi showed a general 
thickening of their walls, with fl^Tt tumors projecting inward. The 
new growth was composed of a stroma enclosing cavities filled with 
cells. The cells were small, nucleated, polygonal or cylindrical in 
shape, and packed closely together. Apparently the new grv>\vth 
originated in the mucous glands. 

Other cases of primary carcinoma of the bronchi are described 
by several authors. ' 

1 Virchow's Arch., liii., p. 470. Virchow's Arch., Bd. Ivi.. Bd. Ixxxv. Arch. d. 
IToilkunde, xix. Prag-er mod AVochenschr., 1883. Zcitsch. f . Heilkimde. v. Trans, 
bond. Patli. Soc, xl. and xli. 

ol 



354 THE RESPIRATORY SYSTEM. 

Sarcomata of the walls of the bronchi occur as secondary 
growths, and as extensions of similar growths in the mediastinum. 
Primary sarcoma of the bronchi seems io be rare. Hesse ^ describes 
a form of lympho-sarcoma forming nodules around the bronchi as 
of common occurrence among the miners in some cobalt and nickel 
mines. 

THE LUNGS. 
MALFORMATIONS. 

One or both lungs may be entirely wanting or only partially de- 
veloped. In some of the cases with only one lung the patients have 
grown up to adult life. 

A peculiar degeneration, by which the lung is converted into a 
number of sacs containing air and serum, the sacs communicating 
with the bronchi, has been seen in a few instances. 

The lobes may be subdivided by deep fissures. An accessory 
lobe, separated from the lung, between the base of the left lung and 
the diaphragm, has been described by Rokitansky. 

There may be hernia of the lung, with absence of part of the 
wall of the thorax. 

There may be transposition of the lungs, with similar changes in 
the position of the heart and the abdominal viscera. 

INJURIES — PERFORATIONS. 

Severe contusions of the thorax may produce rupture of the 
lungs, w^th extravasation of blood into the pleural cavities. 

The lungs may be wounded by a fractured rib and by penetrat- 
ing weapons and projectiles. Such injuries often produce bleeding 
into the lung tissue and inflammatory changes. The lungs, how- 
ever, exhibit a considerable degree of tolerance for such injuries, and 
the patients often recover. 

Collections of pus in the pleural cavities, the mediastinum, the 
liver, the spleen, the kidneys, and the peritoneal cavity may per- 
forate the lungs. Abscess of the lung may be secondary to liver ab- 
scess from amoeba coli. 

CONGESTION AND CEDEMA. 

These two conditions are regularly associated Avith each other in 
the lungs, although one or the other of them may preponderate in 
different cases. 

A moderate degree of congestion and oedema of the posterior por- 
tions of the lungs is often found as a result of post-mortem changes. 

'Arch., f. Heilkunde, xix., p, 160. 



THE RESPTKATORY SYSTEM. 355 

In persons who have been comatose from any cause for some 
hours before death, congestion and cjedema of the lungs are regularly 
developed. 

With disease of the heart, kidneys, and lungs the congestion, 
and especially the oedema, may be excessive. The lungs may be so 
completely infiltrated with serum as to be unaerated. Such a solid 
oedema of the lungs is sufficient of itself to cause death. It has 
been asserted by Welch ^ that the cause of such an excessive oedema 
is a paralysis of the left side of the heart, while the force of the 
right heart is unimpaired. Such an explanation seems to be plau- 
sible. 

Patients confined to bed for a considerable length of time may de- 
velop congestion of the dependent portions of the lungs — hypostatic 
congestion. The affected portion of lung is shrunken, congested, 
and imperfectly aerated. 

HAEMORRHAGE. 

Extravasations of blood within the air cavities are found ^\dth the 
general diseases which produce a disposition to bleeding in different 
23arts of the body. 

Blood from the bronchi or from cavities may be inspired into the 
air vesicles. 

Valvular lesions of the heart, especially of the mitral valve, are 
often accompa-nied by the production of haemorrhagic infarctions in 
the lungs. These infarctions are circumscribed, of rounded or 
wedge-shaped forms, from the size of a walnut to that of an orange. 
They are of dark-red color, unaerated, the air passages distended 
with blood, and are often surrounded by a zone of pneumonia. 
They may be situated in any part of the lungs, but are most com- 
mon in the lower lobes. When they are near the surface of the 
lungs a circumscribed pleurisy is often produced. 

Such infarctions may produce death ; they may become gangre- 
nous, or the blood may becoine absorbed, or they may be gradually 
changed into a smaller mass of pigmented fibrous tissue. 

It is probable that these infarctions are produced either by throm- 
bosis of branches of the pulmonary artery or by rupture of the capil- 
laries. 

Infarctions of smaller size, and with more disposition to be sur- 
rounded by inflammatory changes, are produced by emboli from tlu^ 
right side of the heart and from thrombi in the veins of pviBuiic pa- 
tients. These infarctions are usually situated near the surface of the 
luiliT. '^ 



• Virchow's Arcliiv., 72. 

- Kccciit studios on lung infarctions have boon nindo by Graicit:, ' Festsohrift " for 
Virchow's 71st birthday, 1891. 



356 THE RESPIRATORY SYSTEM. 

Haemorrhages with rupture of the king tissue are produced by 
severe contusions, by penetrating wounds, and by the rupture of 
aneurisms. 

EMPHYSEMA. 

Emphysema is of two kinds — interlobular and vesicular. 

Interlohular Emphysema is produced by the rupture of air spa- 
ces and the escape of air into the interstitial tissue of the lung. 
Or the pulmonary pleura may also be ruptured and the air escape 
into the pleural cavity, or into the mediastinum and from thence into 
the neck. Such a rupture of the air spaces is most frequently caused 
by broncho-pneumonia with consolidation of portions of the lungs. 

Vesicular Empliysemai^ a dilatation of the air jDassages and vesi- 
cles of the lungs. A temporary emphysema can be produced in a 
variety of ways. The bronchi may be obstructed in such a way that 
the air can enter the air spaces, but cannot escape from them. A 
portion of the lungs may be consohdated or compressed, and then 
the air spaces of the rest of the lungs will be dilated. Death may 
take place, Avith a dilatation of the lungs which remains after death. 

Permanent emphysema may change an entire lung if the other 
lung becomes permanently unaerated : it may change portions of a 
lung if other portions are consolidated. 

'''Substantive emphysema'' is a term which is now used in a 
clinical rather than in an anatomical sense. It is used to designate 
a group of cases in which there are regularly developed changes m 
the shape of the thorax, certain characteristic physical signs, a ha- 
bility to bronchitis, to constant and spasiaiodic dyspnoea, to venous 
congestion of the viscera and of the skin. In patients who present 
such symptoms during life, we find after death diffuse changes of 
both lungs, of which dilatation of the air spaces may form a part. If 
the dilatation of the air spaces does exist, the term ' "' substantive 
emphysema " is appropriate : if it does not exist ttc employ a term 
which contradicts itseK. 

The real lesion of substantive emphysema is a chronic productive 
inflammation of the luno- ^vith the formation of new connective tis- 
sue — a process analogous to similar chronic inflammations of the en- 
docardium, arteries, and kidneys, and one which, like them, may 
constitute a formidable disease or an unimportant senile change. 

Both lungs are moderately or considerably increased in size. Very 
often they are partly covered by connective-tissue pleuritic adhesions. 
The mucous membrane of the bronchi may be coated T\rith mucus or 
with muco-pus. The muscular coat of the bronchi may be thick- 
ened ; their entu-e wall may be tliickened or thinned and infiltrated 
with cells ; they may be narrowed or dilated ; they may be sur- 
rounded by zones of pneiunonia. The cells which line the Avails of 



THE KESPIRATORY SYSTEM. 357 

the air spaces are increased in size and number. The walls of the 
air spaces are more or less thickened, except in the case of some of 
the air spaces which are dilated. In the walls of some of the air 
spaces, those which are thickened as well as those which are thinned, 
are formed small holes (Fi<^. 17G) which may later reach a large 
size, so that adjacent air spaces become fused together. 

In some cases of substantive emphysema no dilatation of the air 
spaces exists. In many of the fatal cases the dilatation is but 
moderate ; in some cases it is very marked. The dilatation may 






\ /'-F^' 



m 



•• /O; /. • 



Fig. 176.— Emphysema, showing Holes in the Walls op the Air Vesicles, x SoO and reduced. 

From a case of chronic miliary tuberculosis. 

involve the air passages alone, or both the air passages and the 
vesicles. It is not uniform, but involves some parts of the lungs 
more than others. 

The arteries throughout the lungs and in the walls of the larger 
])ronclii may have their coats thickened. The capillaries in tlu^ 
walls of the air spaces which are but little dilated are unchaiigeil. 
Those of the dilated air spaces are separated by wider intervals : 
they may be smaller ; it is said that they may be obliterated. 

The right ventricle of the heart may be dilated or hypertrophied 
or both. Tliere may be veiious congestion o^ t1ie pia mater, thv 



358 THE RESPIRATORY SYSTEM. 

stomach, the small intestine, the hver, the spleen, the kidney's, and 
the skin. There mav be dropsv. 

ATELECTASIS. 

A collapsed and nnaerated condition of portions of lung tissue is 
either congenital or acquired. 

1. In congenital atelectasis portions of the lung are firm, non- 
crepitant, of a dark-blue or purple color, depressed and smooth on 
section. These portions can usually be artificially inflated, and then 
cannot be distinguished from the surrounding pulmonary tissue. 
This condition is produced by the inability of the child after birth to 
fully mflate its lungs, either from want of sufficient vitality or from 
obstruction of the bronchi. If the child lives for some time, and the 
collapsed lobules are not inflated, thev become hard and dense. 

2. In young children the smaller bronchi may become ob- 
structed by the inflammatory products of bronchitis and the corre- 
sponding air vesicles ^vill then collapse. We then find scattered 
through the lungs collapsed lobules like those in the new-born child. 
Inflammatory changes may be subsequently developed in the col- 
lapsed lobules. 

3. In adults, large or small portions of lung tissue may become 
collapsed as the result of bronchitis, of stenosis of a large bronchus, 
of compression of a bronchus, of paralysis of the pneumogastric, of 
compression of the lungs by fluid or by new growths, and of, long- 
continued feebleness of the act of respiration. 

GAXGREXE OP THE LUNGS. 

It is customary to distinguish two forms of gangrene of the lung, 
the circumscribed and the diffuse ; yet both can occur together. 

Circumscribed gangrene occurs in the form of one or more 
rounded or irregular masses of variable size. The gangrenous por- 
tion of lung is at first brown and dry. The surrounding lung tissue 
is congested or oedematous, or infiltrated with blood, or infiamed. 
If the gangrenous focus is near the pleura the latter will be coated 
with fibrin. Gradually the gangrenous portion of lung assumes a 
dirty-green color and a putrid odor. It becomes soft, broken down, 
and separated from the surrounding lung. The blood vessels may 
be obliterated by thrombi, or eroded, so that there are profuse haemor- 
rhages. 

Such a gangrenous process may extend to the adjacent lung tis- 
sue, or a zone of gray or red hepatization or of connective tissue may 
be formed. 

The fluid from the gangrenous lung may pass into the bronchi 



THE RESPIRATORY SYSTEM. o6U 

and be expectorated ; or it may run from one bronchus intcj another 
and set up new gangrenous foci or diffuse gangrene. 

The pulmonary pleura may be perforated and a gangrenous pleu- 
risy produced. 

Diffuse gangreue may follow the circumscribed form ; it may 
complicate lobar pneumonia or occur as an idiopathic condition. A 
large part of a lobe or of an entire lung becomes greenish, putrid, 
and soft, and the pulmonary pleura is inflamed. There may be ha3m- 
orrhages from eroded vessels. There may be general septicaemia. 

Various forms of bacteria may be present in gangrenous areas of 
the lungs. Among those frequently present is the Staphylococcus 
pyogenes aureus. 

PNEUMONIA. 

The inflammations of the lung, as distinguished from those of the 
bronchi and pleura, are called "pneumonia.^' 

In the present state of our knowledge the classification of the 
different forms of pneumonia must be an arbitrary one. We de- 
scribe separately : 

Acute lobar pneumonia. 

Broncho-pneumonia. 

Secondary and complicating pneumonia. 

The pneumonia of heart disease. 

Interstitial pneumonia. 

Tubercular pneumonia. 

Syphilitic pneumonia. 

I. Acute Lobar Pneumonia. 

This is an acute exudative inflammation, which involves regu- 
larly the whole of one lobe, or the larger part of one lung, or por- 
tions of both lungs. It is an infectious inflammation, attended with 
the growth in the lung of pathogenic bacteria — most frequently the 
" Diplococcus pneumoniae '" of Frankel, less frequently the bacillus 
described by Friedlander. Apparently there are also irregular forms 
of lobar pneumonia attended with the growth of other species of bac- 
teria. 

The inflammation is of pure exudative t^-^^e, characterized by 
congestion, emigration of white blood cells, diapedesis of red blood 
cells, and exudation of blood plasma, while the tissue of the lung 
itself is but little changed. 

During the first hours of the inflammation, only irregular por- 
tions of the lobe which is to be inflamed are involved : later the en- 
tire lobe. The lung is congested, o?dematous, tough, but not con- 
solidated. The air spaces contain granular matter, fibrin, pus cells. 



360 



THE RESPIRATORY SYSTEM. 



red blood cells, and epithelial cells. The epithelium remaining on 
the walls of the air spaces is swollen ; there are large numbers of 
white blood cells in the capillaries. The larger bronchi are con- 
gested, dry, or coated with mucus ; the small bronchi contain the 
same inflammatory products as do the air spaces. The pulmonary 
pleura, as a rule, is not coated with fibrin. This is called the stage 
of * ' congestion. '^ The stage of congestion regularly only lasts a few 
hours, but it may be protracted for several days. 

When the exudation of the inflammatory products has reached 










ii.: 



Fig. 177.— Acute Lobar Pneumonia— Red and Gray Hepatization, x 850 and reduced. 
Showing the pneumococci of Frankel in the exudation, stained yiolet. 

its full development the presence of these products within the air 
spaces and bronchi causes the lung to be solid, and at this time the 
lung is said to be in the condition of ^'red hepatization.'' The lung- 
is now consolidated, red, its cut section looks granular, the granules 
corresponding to the plugs of inflammatory matter within the air 
spaces. For some time after death the inflammatory products re- 
main solid and the cut section of the lung dry ; but later, with the 
commencement of post-mortem changes, these products soften and 



THE RESPIRATORY SYSTEM, 



:j(;] 



the cut section is covered with a grumous fluid. The air vesicles, the 
air passages, the small bronchi, and sometimes the large bronchi, are 
tilled and distended with fibrin, pus cells, red blood cells, and epithe- 
lium, and may contain large numbers of bacteria (Fig. 177). In 
spite of the pressure on the walls of the air spaces the blood vessels 
in their walls remain pervious. The pulmonary pleura is coated 
with fibrin and the interstitial connective tissue of the lung is infil- 
trated with fibrin. The hepatized lobe is increased in size, some- 
times so much so as to compress the rest of the lung. About one- 
fourth of the fatal cases die in the stage of red hepatization at any 
time from twenty-four hours to eleven days after the initial chill. 









•(<-,■ 












^.^m. iMM'i'-' 






'^^■s^KfMs?;. ■'■■ 



im'-f.'/o'Ws^s^S^-'- ■■ ■■■' 





■ , .•;=!?;-.: -A* •'^sfw-'; 



■^^ 




Fig. 178.— Acute Lobar Pneumonia with the Production of Organized Tissue in the Am 
Spaces, x 130 and reduced. 

The section shows a number of air vesicles containing organized tissue. 



After the air spaces have become completely filled with the exu- 
dation, if the patient continues to live, there follc^ws a period during 
which the exudate becomes first de(»olorized and then degenerated. 
This is the period of **gray hepatization." The lung remains solid, 
its color changes, first to a mottled red and gray, then to a uniform 
gray. The coloring matter is discharged from the red blood cells 
and the exudate begins to degenerate and soften. The lung is found 
passing from red to gray hepatization at any time between the 

Olil 



362 



THE RESPIRATORY SYSTEM. 



second and the eighteenth day of the disease. It is found com- 
pletely gray at any time from the fourth to the twenty -fifth day. 
About one-half of the cases die in the condition of mo'ttled red and 
gray hepatization ; about one-fourth in the condition of gray hepa- 
tization. 

If the patient recovers the exudate undergoes still further de- 
generation and softening and is removed by the lymphatics. This 
is the stage of " resolution. ^^ It should commence immediately after 




Fia. 179.— Organized Tissue in an Air Vesicle, x 850 and reduced. 



defervescence and be completed within a fevv^ days. But it may not 
begin until a number of days after defervescence, or it may be un- 
usually protracted. 

The pneumococcus of Frankel (often also called the Diplococcus 
pneumonise of Frankel) is the bacterium most often present in the 
lungs in acute lobar pneumonia, and the form which there is much 
reason to believe, in the large proportion of cases, to be the cause of 
the disease. The germ is described on page 162. 

There is a form of lobar pneumonia in which the inflammation is 
not simply an exudative one, but there is also a growth of new con- 



THE RESPIRATORY SYSTEM. 



363 



nective tissue in the walls of the air spaces and in their cavities 
(Fig. 178). 

This condition has been usually described as a chronic inflam- 
mation following an ordinary lobar pneumonia. It seems really to 
be from the outset a special form of pneumonia. For we find, in 
patients who have not been sick for more than a few days, that the 
pneumonia already has . its characteristic form. Still further, even 
in its earlier stages the clinical history is somewhat different from 
that of an ordinary lobar pneumonia. 




Fig. 180.— Air Vesicles containing Organized Tissue in Lobar Pneumonia, \ 350 and reduced. 

The blood vessels are injected. 



If the patient dies within three weeks of the commencement ot 
the pneumonia we find one or more lobes consolidated but not much 
enlarged. The hepatization is smooth and dense. The walls of the 
air spaces are thickened and coated with an increased number of 
epithelial cells. Some of the air spaces contain onl}' fibrin and pus, 
but in others there is new connective tissue, basement substance and 
cells (Fig. 170). In this new tissue there may be new blood vessels, 
which can be artificially injected from the vessels of the liiui;- (Fig. 
180). 



364 THE RESPIRATORY SYSTEM. 

If the patient lives for several months we find the lung very 
dense and smooth. The growth of new connective tissue is more ex- 
tensive, the air spaces are completely filled, their walls are much 
thickened, and in some places the lung tissue is completely changed 
into smooth connective tissue. 

II. Broiiclio-pneuinonia {Capillary Bronchitis, Lobular Pneu- 
monia, Catarrhal Pneumonia). 

This is the ordinary pneumonia of young children ; it is frequent 
also in young persons, but not as common in adults. 

In children it seems to be due to the same causes which produce 
lobar pneumonia in adults : to the poisons of the different infectious 
diseases ; to the inhalation of irritating substances and gases, and of 
the bacteria which produce suppuration. 

In adults the disease may present itself to us in a variety of ways. 

1. The patients have an ordinary attack of catarrhal bronchitis 
lasting for several days. Instead of getting well promptly, how- 
ever, the patients continue to cough and to feel sick, and on examin- 
ing the chest we found a circumscribed area where there is dul- 
ness on percussion and loud, high-pitched voice. This consolidation 
of the lung does not, however, last very long, and the patients 
make a good recovery. 

2. The patients are suddenly attacked with a very severe and 
general broncho-pneumonia. There are chills, a rapid rise of tem- 
perature, headache, pains in the back and chest, vomiting, great 
prostration, a rapid pulse which soon becomes feeble, very bad 
breathing — rapid, labored, and insufficient — venous congestion of the 
skin and of the viscera, cough, at first dry, then with profuse mucus 
and blood-stained sputa, sleeplessness, restlessness, and delirium, 
and albumin in the urine. There are coarse subcrepitant and crepi- 
tant rales over both lungs, sibilant and sonorous breathing ; the per- 
cussion note is normal, or exaggerated, or dull. The disease lasts 
for from seven to fourteen days, and is very apt to prove fatal. 

3. There is a form of broncho-pneumonia in adults which re- 
sembles lobar pneumonia. There is a general catarrhal bronchitis, 
with broncho-pneumonia and consolidation of one or more lobes. 
The symptoms and physical signs are like those of lobar pneumonia, 
but with some difference. The invasion of the disease is not as sud- 
den, the pulse is more rapid, the cerebral symptoms are more con- 
stant, the expectoration is like that of bronchitis, the physical signs 
are more slowly developed, the duration of the disease is rather 
longer and resolution is slower. 

4. There is a form of broncho-pneumonia which resembles acute 
phthisis, The patients have a cough with expectoration, at first 



THE RESPIRATORY SYSTEM. 



36o 



mucous, afterward muco-purulent. There is a moderate fever, with 
evening exacerbations and sweating at night. The patients steadily 
lose flesh and strength. The physical signs are those of bronchitis 
and of consolidation of parts of the lung. The disease is protracted, 
continuing as long as ten weeks, and is apt to prove fatal. 

With substantive emphysema there may be developed a subacute 
or chronic broncho-pneumonia. 







r 











V-_y 



\rf^f' 



^^i.i^', 



) ^- 






a-' 



rz 






^/, 



I 



1 



( 



V 



r^( 



J 



-^%. 



3) 
-J 










,\> .1, , /^^>( 

Fig-. 181,— Broncho-pneumonia in a Child, x 750 and reduced. 
Air vesicles in diffuse hepatization. 

The essential or constant lesion of broncho-pneumonia is an in- 
flammation of the walls (not the mucous membrane) of the bronchi 
and of the air spaces immediately surrounding the inflamed bronchi. 
The walls of the bronchi are thickened and infiltrated by a grcnvtli 
of new cells. The walls of the air spaces are thickened, their cavi- 
ties are filled with fibrin, pus, and epithelium or with new comiec- 
tive tissue. The inflammation, involves the medium-sized and 
smaller bronchi of both lungs, butis not everywhere equally severe : 
in some parts of the lungs the lesions avo much more marked than 



366 



THE EESPIRATORY SYSTEM. 



in Others. In some of the cases there are no other changes except 
some general congestion of the Imigs. In other cases there may be 
added a catarrhal inflammation of the mucous membrane of the 
bronchi, diffuse consohdation of parts of the lung, pleurisy, dilata- 
tion of the inflamed bronchi, areas of atelectasis, simple or tubercu- 
lar inflammation of the bronchial glands. 

The trachea and the larger bronchi are congested and coated with 
mucr.s. The smaller bronchi contain pus, their walls are thickened 
and infiltrated with cells, and thev mav be dilated. Around manv 







^^/,:^^ 










/■/' 



Fig. 181— Broxcho-fntx^onia ix ax Adttlt. x 850 and reduced. 
An air vesicle containing organized tissue in a zone of peribronchitic pneumonia. 



of the small bronchi are narrow zones of congestion or hepatization 
The rest of the lungs is congested and oedematous. 

Or the zones of peribronchitic pneumonia are larger, so that a sec- 
tion of the lung is mottled with httle whitish nodules, each nodule 
corresponding to a cut bronchus surrounded by its zone of pnemnonia. 

Or between these zones of peribronchitic pneumonia are areas of 
diffuse hepatization which render portions of the lung completely 
sohd (Fig. 181). 

Or there may be areas of atelectasis corresponding to occluded 
bronchi. 



THE RESPIRATORY SYSTEM. 



3G7 



There is often a thin layer of fibrin on the pulmonary pleura. 
The bronchial glands are the seat of simple or tubercular inflamma- 
tion. 

The dilatation of the bronchi ig not constant. When present it is 
of the cylindrical character and involves the medium-sized bronchi 
for a considerable part of their length. Such dilated bronchi are 
each of them surrounded by a narrow zone of pneumonia ; the inter- 
vening lung tissue may be still aerated or hepatized. 

In these peribronchitic zones of pneumonia the thickening and 
cellular infiltration which exist in the walls of the bronchi extend 




Fig. 183.- Persistent Broncho-pneumonia. 

also to the Avails of the air spaces. These walls are thickened and 
infiltrated with cells, while the cavities of the vesicles are filled with 
pus and epithehum or with tissue resembhng granulation tissue (Fig. 
182). In the diffuse hepatization the air vesicles are filled with 
epithelium, pus, and fibrin in vaiying proportion and quantity : the 
Avails of the air spaces remain unclianged. 

Tlio portions of lung which are not hepatized are congested and 
(edematous. Tlie cavities of the vesicles are diminished by the en- 
larged capillaries, tlie epithehum is SAvollen, anil i:i many Vesicles a 
few pus or epithelial cells ai-e to be found. 



% 



368 



THE RESPIRATORY SYSTEM. 



Sucli a bronclio-pneumonia differs from the ordinary lobar pneu- 
monia Yery decidedly. The inflammatory process is not a superfi- 
cial one, resulting only in filhng the bronchi and air spaces with in- 
flammatory products, but it affects also the tissue of the lung, infil- 
trating the Trails of the bronchi and of the air spaces. 

This interstitial character of the inflammation seems to be the 
reason why the disease is often protracted and sometimes succeeded 
by a chronic inflammation. This chronic condition we ^ylU call 
" Persistent Broncho-pneiunonia.'^ 







S5^ ^K^;^ 



wA 




M 



^:- 



M 



f ■■•'-- 



^ ■■- 



M 


















Fig. 184.— Peesistext Broncho-pneumonia. 

The original acute broncho-pneumonia is succeeded by a chronic 
inflammation involYing especially the interstitial tissue. 

This inflammation maY IuyoIyg ouIy some of the smaller bronchi 
and small zones of Yesicles around them, and then a section of the 
lung will seem to be studded with fibrous nodules (Fig, 183). Or all 
the bronchi of sorae part of the lung "\Yill be inflamed, the peribron- 
chitic zones of pneumonia wfll become continuous, and so part of a 
lobe or an entire lobe become conYerted into a dense mass of con- 
nective tissue. The air vesicles are obliterated by the new connec- 
tive tissue, the interlobular septa and the palmonary pleura are 
thickened (Fig. 184), and the inflamed bronchi may be dilated. The 
blood vessels, however, are, for the most part, not obliterated, so 



THE RESPIRATORY SYSTEM. 



369 



that the lung does not become necrotic or degenerated, although 
occasionally areas of cheesy degeneration exist. 

III. Secondary and Complicating Pneumonia, 

Inflammation of the lungs occurs frequently as a complicating 
condition with lesions of the brain and spinal cord, with pysemia, 
with the continued fevers, after injuries and surgical operations, and 
in patients who are confined to bed for a long time from any cause. 

The pneumonia developed in these cases may follow one of two 
different types. 




Fig. 185. — Lobular Pneumonia in a Child, complicating Diphtheria. 

Air vesicle showing inflammatory products and large numbers of bacteria (streptococci) 
stained with methyl violet. 



1. Part of the lung, usually the posterior portion, is congested, 
leathery, only partly aerated, and mottled by irregular patches of 
red or gray hepatization which have no relation to the bronchi. In 
the hei)atized portions of the lung the air spaces are filled with pus 
and fibrin. 

2. The inflammation has the characters of a broncho-pneumonia. 
The small bronchi are filled with pus, their epithelium is altorod, 
their walls are infiltrated with pus. and around each bronchus is a 
zone of air vesicles filled with pus and fibrin. The lung is mottled 

m 



370 



THE KESPIRATORY SYSTEM. 



with little whitish nodules, corresponding to the bronchi and the 
peribronchitic zones, and between these there may be a diffuse hepa- 
tization. 

In children suffering from diphtheria, with pseudo-membranes 
containing pathogenic bacteria in the fauces and upper air passages, 
a secondary pneumonia may apparently occur as the result of the 
entrance into the lung spaces of the germs from above (Fig. 185).' 
Although the pyogenic bacteria are the most frequent inciters of 
secondary and complicating pneumonia, other forms of germs are 
capable of inducing it. 



/^•;r":i^ 




Fig. 186.— The Pneumonia of Heart Disease, x 850 and reduced. 
An air vesicle from a child's lung. 



IV. The Pueumonia of Heart Disease. 

Lesions of the aortic and mitral valves, and dilatation of the left 
ventricle, often produce a diffuse, chronic inflammation of both lungs 
of a peculiar character. This condition is often called pigment in- 
duration, or brown induration, but it is really a chronic pneumonia. 

The lungs are diminished in size and of a peculiar yellow-pink 
color, mottled with spots of black or brown pigment. They are not 
congested, but are of a dry, leathery consistence ; or portions of them 

^ Consult Prudden and Northrup, " Studies on the Etiology of Pneumonia com- 
plicating Diphtheria in Children," American Journal of Medical Sciences, June, 1889^ 



THE RESPIRATORY SYSTEM. 



3?L 



may be in the condition of a smooth red hepatization. The appear- 
ance of these lungs may be modified by the presence of hsemorrhagic 
infarctions, by the pre-existence of emphysema, or by cedema. 

Minute examination of these lungs shows four separate pathologT- 
cal conditions. 

1. A change in the capillaries in the walls of the air spaces. 
These capillaries are dilated and tortuous, so that they project int<j 
the cavities of the vesicles. The degree of the dilatation varies in 
the different lungs ; in some it is very marked, in others but light. 

2. A thickening of the walls of the air spaces, due partly to the 



KJ^...^ ^^^' 







'^S^*'*.^ 



Fig. 187.— Interstitial Pneumonia, x 90 and reduced. 
From a case of chronic phthisis. 



dilatation of the capillaries, partly to a growth of smooth muscle, 
and partly to a growth of connective tissue. The degree of the 
thickening varies very much in different cases. 

3. A formation of black or brown pigment in the shape of gran- 
ules and small masses. This is deposited in the walls of the vesicles, 
in the interstitial connective tissue, and in the new cells ^^'ithin the 
vesicles. 

4. A formation of cells within the air spaces. The walls t>f tlu^ 
vesicles are coated with a layer of flat, nucleated cells. Similar cells, 
or swollen and granular cells, are present in the cavities of the 
vesicles (Fig. ISO). If these cells are numerous the cavities of the 
vesicles are filled, and there results a smooth red hepatization. 



372 



THE RESPIRATOKY SYSTEM. 



V, Interstitial Pneumonia. 

Moderate degrees of inflammation of the lung, with the produc- 
tion of interstitial connective tissue, are common. Such a develop- 
ment of interstitial pneumonia as to constitute a disease by itself is 
comparatively rare. 

Causes. — Well-marked interstitial pneumonia follows attacks of 
broncho-pneumonia ; severe attacks of pleurisy which leave behind 




Fig. 188.— a Miliary Tubercle, x 300 and reduced. 

Involving only two air vesicles, of which the walls are infiltrated and the cavities filled with 
tubercle tissue. The blood vessels of the air vesicles are injected. 



extensive adhesions ; chronic bronchitis ; and the inhalation of the 
dust of coal or stone. 

Lesions. — The inflammatory changes are regularly confined to 
one lung, except in the cases of inhalation pneumonia. This lung- 
is thickly covered with old adhesions, its pulixionary pleura is 
thickened ; the lung itself is small. Bands of dense fibrous tissue 



THE RESPIRATORY SYSTEM. 



d7'd 



extend from the pleura into the lung. There is a growth of con- 
nective tissue in the septa between the lobules, around the bronchi 
and the blood vessels, and in the walls of the air spaces (Fig. 187). 
The cavities of the air spaces are compressed and obliterated. The 
mucous membrane of the bronchi is the seat of chronic catarrhal in- 
flammation. The walls of the bronchi may be thickened and their 
lumen narrowed ; or their walls may be thinned with the formation 
of bronchiectasise. 




MS' 

Fig. 189.— a Miliary Tubercle, x 330 and reduced. 

Formed of several air vesicles filled with tubercle tissue and surrounded by a zone of tissue 
resembling granulation tissue. 

The other lung is large and emphysematous. 

Suppurative interstitial pneumonia is sometimes produced in cases 
of septictemia. The pulmonar}^ pleura is coated with flbrin, the 
bronchi contain pus, portions of the lung are hepatized, and the in- 
terlobular septa are infiltrated with pus. 

VI. I'fihrrcfdar Piwfnnoiiia. 
The lungs may IxMHiine the seat of tubercular intiainmation a< 



374 THE RESPIEATuRY SYSTEM. 

part of tlie lesions of an acute general tuberculosis^ or tliey may be 
affected by localized tubercular in£cinunations. 

The localized tubercular inflammations may conveniently be de- 
scribed im.der the names of : Acute miliary tuberculosis ; Subacute 
miliary tuberculosis ; Chronic mihary uiberculosis ; Acute phthisis 
and Chronic phthisis. 

Acute Miliary TiLbercidosis. — The acute development of mHiaiy 
tubercles in the lungs is usually only part of general tul>erculosis. 
althouo:h the lesion mav be most extensive in the lunsrs. 

Both lungs are usually involved, but the distribution, number, 
size, and character of the miharv tubercles differ in different cases. 








Fig. 190. — A Miltabt Tubeecle, X 300 and reduced. 
Formed of a number of air vesicles, some contaming tubercle tissue, others pus and epithelium. 

The larger bronchi are the seat of catarrhal inflammation : the 
lung tissue is congested ; the air spaces contain ei:»ithehum. pus, and 
fibrin in small quantity. 

The tubercles are found in the parenchyma of the lung, in the 
connective tissue forming the septa, along and in the walls of the 
bronchi and bl-jod vessels, and in the pulmonaiy pleura. 

Thev are scattered sin2:lv throusrh the lunsrs. or aaroresrated in 
groups. They may be separated by considerable interspaces, or so 
close together that the lung is rendered nearly sohd. Some are so 
small and transparent that they can hardly be seen vrith the naked 
eye ; others are larger and more opaque. In chfldi-en's lungs large 
masses are found of the same structure as miharv tubercles. 



THE RESPIRATORY SYSTEM. 



375 



When we examine miliary tubercles as they exist in different 
lungs, it becomes evident that they are not all of the same structure. 
We find . 

1. Miliary tubercles composed entirely of amorphous granular 
matter, with a few shrunken cells and an external zone of pus cells. 
These cannot be said to have any definite anatomical structure. 
In some of them the outlines of the walls of the air spaces are still 
visible ; in others they are lost in the cheesy mass. 




Fig. 191. —A Peiubronchitic Miliary Tubercle. 



2. Miliary tubercles composed of a group of air spaces of which 
the Avails are infiltrated and the cavities filled (Fig. 188). The walls 
of the air spaces are infiltrated with granulation tissue or tubercle 
tissue ; as the infiltration progresses the blood vessels are obliterated. 
Such an infiltration may involve symmetrically the whole of the 
wall of an air space, or only a portion of the wall. The cavities of 



376 



THE RESPIRATORY SYSTEM. 



tlie air spaces are filled with tubercle tissue, or with epithelium, 
fibrin, and pus. 

In some of these tubercles the tubercle tissue, both in the walls 
of the air spaces and in their cavities, is well developed (Fig. 189) ; 
then they look like little tumors replacing the lung tissue. In 
others the outlines of the walls of the vesicles are preserved, granu- 
lation tissue predominates, the cavities of the vesicles contain pus, 
epithelium, fibrin, and less tubercle tissue (Fig. 190) ; then the tu- 
bercles look like little areas of a composite hepatization. 




Fig. 192.— Miliary Tubercle in Lung of Child. 
Showing the Bacillus tuberculosis— stained with fuchsin— in the contents of the air vesicles and 
in their thickened walls. (The size of the bacilli relative to other elements is slightly exaggerated.) 

In adults such tubercles are small, but in children they may 
reach a large size. 

3. Miliary tubercles formed by the infiltration of the wall of a 
bronchiole or air passage with tubercle tissue or granulation tissue. 
This infiltration is apt to involve only one side of the bronchiole or 
air passage. It may be confined to this or it may extend to the 
walls of the adjacent vesicles. These vesicles may remain empty, 
they may be dilated, or they may be filled with tubercle tissue or 
with epithelium, fibrin, and pus. 



THE RESPIRATORY SYSTEM. 



377 



4. Miliary tuberck^s formed by the infiltration of the walls of 
small bronchi with tubercle tissue or granulation tissue (Fig. 191). 
The infiltration often extends to the surrounding air spaces, so as 
to form tubercles of large size. 

In all these miliary tubercles there is often cheesy degeneration 
of the central portions. 

Tubercle bacilli can . be demonstrated in most of these miliary 
tubercles, especially in those which have undergone cheesy degene- 
ration (Fig. 192). 

Subacute Miliary Tuberculosis, — The disease involves only the 
apex of one lung, or one lobe, or portions of both lungs. The inflam- 
mation may continue for weeks or months, then stop and the patient 



if \^^^( V-:' ^ 




k 



:?-7^^'^^T-.« 



^*ris---5V 



r\.*T 













Fig, 193.— An Ag«regation op Miliary Tubercles, X 90 and reduced. 

recover. Or the patient may have a number of attacks, from each 
one of which he recovers. Or the disease may continue, extend, and 
cause death within a few months. Or it may be succeeded by chronic 
miliary tuberculosis. 

The miliary tubercles are small. ]\Iost of them are formed within 
the air spaces or around the bronchioles. They are composed princi- 
pally of tubercle tissue or of round-celled tissue. In the portioTi i^f 
lung where the tubercular inflammation is Q'oino- on there mav also 
be localized catarrhal bronchitis and })leurisy. 

Chronic Milianj 'Tuberculosis.— The morbid process begins at 
the apex of one lung and then slowl}^ extends, either progressively or 
m attacks, until a large part of the lungs is involved. 
34 



378 THE RESPIRATORY SYSTEM. 

In the simplest form of the disease the only change in the lungs 
is the formation of miliary tubercles. These tubercles are harder 
and denser than those found with general tuberculosis or with sub- 
acute pulmonary tuberculosis. They are composed of tubercle tissue, 
or round-celled tissue, or connective tissue, or are in the condition of 
cheesy degeneration. 

Usually, however, in addition to the miliary tubercles there are 
other changes in the lungs. These additional lesions begin in the 
same part of the lung Avhere the tubercles are formed, and accom- 
pany the development of the tubercles in fresh parts of the lungs. 

There may be a localized catarrhal bronchitis. 

There may be an inflammation of the walls of the bronchi, 'vvith 
















'■^ .-i - 










Fig. 194. — Diffuse Tubbrculae, Inflammation producing Diffuse Consolidation of the Lung, 

X 300 and reduced. 

partial destruction of these walls and the formation of cylindrical or 
sacculated bronchiectasise. The walls of the ca^^ties thus formed 
may be converted into connective tissue, or they may remain suppu- 
rating and necrotic. 

There may be an interstitial pneumonia with the production of 
new connective tissue, the obliteration of the air spaces, and the con- 
sohdation of portions of the lungs. 

There may be dilatation of the air spaces of the portions of the 
lungs which are not consolidated (Fig. 193). 

There may be thickening of the pulmonary and costal pleura, with 
connective-tissue adhesions. 

While the morbid process begins as a localized tubercular inflam- 
mation of the lungs, and often retains throughout this local character. 



THE RESPIRATORY SYSTEM. 



379 



yet it may also happen that from this local lesion other parts of the 
body may be infected . Tubercular laryngitis, and tubercular inflam- 
mation of the solitary and agminated glands of the small intestine, 
often complicate the pulmonary lesion, and sometimes even acute 
general tuberculosis is produced. 

Acute Pulmonary Phthisis (Acute consumption; Acute catarrhal 




9d±X^:.\ 






'Fio. 195.— An Area of Coagulation Necrosis surrounded by a Zone of Pneumonia. 

X 40 and reduced. 

phthisis). — This name is used to designate an acute tubercular in- 
flammation of the lungs combined with other non-tubercular inflam- 
matory changes. 

1. In one or more lobes there may be miliary tubercles and a 
diffuse consolidation, due to the filling of the air spaces with fibrin, 
pus, and epithelium. 

2. There is a tubercular broncho-pneumonia invoh'ing the smaller 
bronchi of one or more lobes, and zones of air spaces surrounding 



380 



THE RESPIRATORY SYSTEM. 







>->^i^ ^ ^" J.:^xii« 



m^/i^'fs 




. .-.Jt^^ fe^^:"-^^ 



Fig. 196. — Tubkkculah IsTLA^iiLiXiox vtith Cheesy DEGE>-ERA.Tio>r abott the Broxchi rs* A^ 

SrS'GLE LOBO^ OF THE LrXG — ACUTE PHTHISIS. 




Fig. 197. —Acute Pctlmokary Phthisis "with TuBEROCiiiB Is'FLAinu.Tiox a>*d Diiatatiox oe^ 

Bronchi. 



THE RESPIRATORY SYSTEM, 



381 



these bronchi. The walls of the bronchi and of the surrounding air 
vesicles are infiltrated with tubercle tissue. 

3. Besides the tubercular inflammation of the walls of the bron- 
chi and of the air spaces surrounding them, there are a general 
catarrhal bronchitis, diffuse consolidation of the lung by the filling 



:tT.i:","T'J 




Fia. 198.— Chronic Phthisis, x 850 and reduced. 
An air vesicle filled with fatty epithelium. 

of the air spaces with fibrin, pus, and epithelium, and fibrin on the 
pulmonary pleura. 

4. Besides the tubercular broncho-pneumonia, the diffuse con- 
solidation, and the pleurisy, there are small or large portions of dead 
lung tissue in the condition of coagulation necrosis (Fig. 105). Those 
areas pass into the condition of cheesy degeneration, and are sur- 
rounded (Fig. lOG) by zones of tubercle tissue or of romul-celled 
tissue ; or they soften cxnd form cavities which are in communication 
with the bronchi. 



382 



THE RESPIRATORY SYSTEM. 







^ L. .J 

Fig. 199.— Chronic Phthisis, x 850 and reduced. 
Showing growth of connective tissue within an air vesicle. 







Fig. 200.— Chronic Phthisis, x 850 and reduced. 
Showing growth of connective tissue within an air vesicle. 



THE RESPIRATORY SYSTEM. 



'J. w •> 
ooo 



5. In addition to the lesions just mentioned, the walls of the 
bronchi are so changed by the tubercular infiammation that cylindri- 
cal or sacculated bronchiectasise are formed (Fig. 197). 

Chronic Phthisis. — The lesions are of the same nature as those 
of acute phthisis, but are modified by the long continuance of the 
inflammation. 

1. The air spaces : 

{a) The air spaces are filled with swollen and fatty epithelium 



ml' 



PV 



I ; ^■ 



v' i-V 




"^i^^^SSuii^^sji^sjrisiss^ 



-^.^3 



Fig, 301.— Chronic Phthisis— Intra-alveolak. Pneumonia. 



(Fig. 198), or with fibrin and pus, while their walls are unchanged 
and their blood vessels remain pervious. 

(b) The air spaces are filled and distended with compact fibrin 
and slnivelled pus and epithelium. Their walls are compressed and 
thin, or thickened and infiltrated Avitli cells. The blood vessels can 
be only very imperfectly injected. This condition may be succeeded 
by complete cheesy degeneration. 

(c) The walls of the vesicles are thickened, their ca\'ities are 
filled with new connective tissue often containing new vessels (Figs. 
199, 200, and 201). This new comiectivo tissue may look like an out- 



384 THE RESPIRATORY SYSTEM. 

growth from the wall of the vesicle, or as if it was formed free in 
its cavity. 

(d) There is a diffuse interstitial growth of fibrous tissue and 
granulation tissue in the walls of the air spaces, the bronchi and the 
blood vessels, and in the septa. By this new tissue the air spaces 
are compressed and deformed or completely obliterated (Fig. 202). 

2. The nodules : 

These, as in acute phthisis, consist of areas of coagulation necro- 
sis, peribronchitic nodules, and miliary tubercles. 



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Fig. 20-2.— lafTERSTiTiAi, Pneumonia of Chronic Phthisis, X 850 and reduced. 

The tubercles may preserve their characteristic structure, or un- 
dergo cheesy degeneration, or be changed into fibrous tissue (Fig. 
203). 

The areas of coagulation necrosis undergo cheesy degeneration, 
or soften and form cavities. They are surrounded by tubercle tis- 
sue, or granulation tissue, or connective tissue (Fig. 204). 

The peribronchitic nodules are much the same as in acute 
phthisis. 

3. The bronchi : 

The changes in the bronchi in chronic phthisis form a very im- 
portant part of the morbid process. 



THE RESPIRATORY SYSTEM. 



385 



(a) The larger bronchi may be the seat of a chronic catarrhal 
inflammation, accompanied by the production of large quantities of 
mucus and pus. 

(b) The bronchi of all sizes may be inflamed, with the produc- 
tion of new cells in their walls, in addition to the inflammatory 
changes of their inner surfaces. Such a cellular infiltration of the 
walls of the bronchi is often followed by dilatation — either fusiform 
or sacculated. 

(c) Tubercle granula and granulation tissue are found in the 
walls of the bronchi. These tissues may degenerate, soften, and thus 
form ulcers. 





^^^^ 




■■-/ 



Fig. 203.— An Old Miliary Tubercle converted into Fibrous Tissue, x 90 and reduced. 

(d) The entire thickness of the wall of a bronchus may become 
the seat of inflammation of a pecuhar character. Tlie surface of 
the mucous membrane is coated with pus, the epithelial layer can 
no longer be seen, the w^all of the bronchus is infiltrated with cells. 
The inflammatory products undergo cheesy degeneration, so that 
we find the inner surface of the bronchus coated with cheesy mat- 
ter, while its wall is also changed into cheesy matter. Such a. con- 
dition of the bronchus is usually followed by sacculated dilatation. 

The cavities of chronic phthisis, therefore, are formed by the 
dilatation of inflamed bronchi, by the softening of areas of coagu- 
lation necrosis, or by the combination of both these processes. 

When cavities are once formed they are apt to continue aiul to 



386 THE RESPIRATORY SYSTEM. 

become larger as the disease goes on. Their walls may be converted 
into granulation tissue, which ulcerates in some places and prolife- 
rates in others ; or portions of the wall become necrotic ; or all ac- 
tive processes cease and the wall of the cavity is formed of new 
connective tissue. The lung tissue between the cavities becomes 
compressed and altered in various ways. As the cavities increase in 
size they touch and open into each other. In this way large portions 
of the lung may be converted into a dense mass honeycombed witk 
cavities. 

■-"--■ \ - 1 













Fig. 204.— Tubercle Tissue around an Akea of Coagulation Necrosis, X 850 and reduced. 

VII. Syphilitic Pneumonia. 

Persons suffering from inherited or acquired syphilis sometimes 
develop inflammations of the lungs which seem to be due to the 
syphilitic infection. The lungs may then be affected in several dif- 
ferent ways. 

1. There is an interstitial pneumonia, beginning around the lar- 
ger bronchi and blood vessels at the root of the lung, and extending 
to the walls of the air spaces and interstitial connective tissue, so that 
the central portions of one or both lungs are converted into a dense 
mass of connective tissue (Fig. 205). 

2. There is an interstitial pneumonia, with the formation of gum- 
my tumors. 



THE RESPIRATORY SYSTEM. 387' 

3. There is an inflammation of the wall of the trachea and of the 
larger bronchi. There are ulcers in the mucous membrane, their 
walls are very much thickened, and their cavities are narrowed or 
dilated. 

4. There are circumscribed areas of interstitial inflammation 
around the smaller bronchi, forming small, hard peribronchitic 
nodules. 

5. There is a diffuse hepatization, involving lobules or an entira 
lobe. The affected portion of the lung is red or white or grayish. 






il>.'; ■; .■• -'■--:.:'-l / 



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Fig. 205.— Interstitial Syphilitic Pneumonia, x 170 and reduced. 



S 



The walls of the air vesicles are infiltrated with cells, and their cavi- 
ties are filled with epithelial cells. 

6. There may be a broncho-pneumonia, like the ordinary broncho- 
pneumonia of children ; or a lobar pneumonia, like that of adults. 

7. There may be an obliterating endarteritis of branches of the 
pulmonary artery, with the formation of white infarctions sur- 
rounded by zones of connective tissue. * 

TUMORS. 
Dermoid cysts have been found in the lungs in a few instances. 
Fibromata have been described by Rokitansky. 

» miUr, Charite Aimalcu, 1894, p. 184. 



4388 THE RESPIRATORY SYSTEM. 

Enchondromata may occur both as primary and secondary tu- 
mors. The primary tumors are small and are believed to originate 
in the cartilages of the bronchi. The secondary tumors often attain 
a very large size. 

Osteoma is very rare. A case is described by Luschka.' 

Sai^comata as secondary tumors are of not infrequent occurrence. 
A primary adeno-sarcoma is described by Weichselbaum. ' 

Lymphomata are found in cases of leukaemia and pseudo-leu- 
iaemia. 






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y 



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Fig. 206.— Primary Carcinoma of the Lung, x 300 and reduced. 

Carcinoma as a secondary growth may have the form of nodules 
or of diffuse infiltration. Primary carcinoma of the lung has been 
described by a number of authors. The new growth (Fig. 206) is in 
the form of small nodules surrounded by pneumonia. As the result 
of the new growth and the pneumonia a considerable part of both 
lungs may be rendered solid. The bronchial glands are infiltrated, 
and there may be secondary nodules in the pleura. 

The new growth seems to originate in the air spaces. Their walls 

^ Virch. Arch., x., p. 500. 
^ Ibid., Ixxxv., p. 559. 



THE RESPIRATORY SYSTEM. 38r^ 

are thickened, their cavities are lined with cyhndrical epitheHum, or 
filled with cylindrical and polygonal cells, some of which undergo 
colloid degeneration. 

Or it may originate in the small bronchi.^ 

PARASITES. 

Echinococci occur in the lungs in their ordinary cystic form. 
The sacs may suppurate and discharge through the pleura, the 
bronchi, the wall of the chest, or the diaphragm. 

In bronchiectasise and in gangrenous cavities in the lungs vege- 
table parasites of various kinds have been described — both moulds, 
and bacteria. 

The Bacillus tuberculosis is regularly found in the walls and con- 
tents of cavities in acute and chronic phthisis, sometimes in enor- 
mous numbers. It is also often present in great numbers in the 
nodules of tubercular inflammation, particularly when these are 
softening and beginning to break down to form cavities (see Tuber- 
culosis). 

THE MEDIASTINUM. 

The anterior mediastinum is situated in front of the pericardium, 
between it and the sternum. At its superior part the two layers of 
pleurae separate somewhat to enclose the vestiges of the thymus 
gland ; behind the second piece of the sternum they are in contact, 
but below this the left pleura recedes from its fellow toward the 
left side, leaving an angular space of some breadth. The triangularis 
sterni muscle bounds this space in front. 

The posterior mediastinum, stretching from the pericardium to 
the bodies of the vertebrae, encloses between its layers the lower part 
of the windpipe and gullet, the thoracic duct, the descending aorta, 
the azygous vein, the pneumogastric nerve, and some lymphatic 
glands. 

INFLAMMATION. 

Suppurative inflammation may occur either in the anterior or 
posterior mediastinum. It may be caused by fractures, caries, or 
necrosis of the sternum and vertebrae, by perforation of the oesopha- 
gus, by suppuration of the Ij^mphatic glands, by pleurisy, or may 
occur without discoverable cause. 

The pus may infiltrate the connective tissue, or may form ab- 
scesses which may attain a large size. The inflammation may ex- 
tend to the pleura or the pericardium , the abscesses may displace 
the heart, the lungs, or the sternum ; or they may perforate through 

^ Virch. Arch., Bd. Ixxxiii., p. 77. 



390 THE RESPIKATORY SYSTEM. 

the skin into a pleural cavity^ the oesophagus, the trachea, or a 
bronchus. 

TUMORS.' 

The most common form of nevr growi^h in the mediastinum is that 
known by the names of lymphoma, lympho-sarcoma, and lymph- 
adenoma. 

These tumors are confined to the mediastinum, or they are asso- 
ciated with similar growths in other parts of the body in the disease 
called "pseudo-leuksemia.^^ 

Persons between the ages of twenty and thirty years seem to be 
the most liable to the growth, but it is also not uncommon in chil- 
dren. 

The growth begins in the lymphatic glands in the mediastinum, 
and at the root of the lung. It increases at first slowly, then more 
rapidly, and gradually infiltrates the adjoining tissues. In this way 
the walls of the trachea, bronchi, and aorta, the pericardium, the 
pleura, and the lung, become infiltrated with the growth. The tumor 
also compresses the surrounding organs. 

The growth is composed of a connective-tissue stroma infiltrated 
with small round cells, the relative quantity of cells and stroma 
varying in the different cases. 

Besides this form of tumor there may also occur in the mediasti- 
num tumors similar to those which grow in the pleura and behind 
the peritoneum — tumors which resemble both the sarcomata and 
carcinomata, and which it is difficult to classify. Aberrant thyroid- 
gland tissue may be found in the mediastinum. 

Teratoma myomatodes. — Under this name Yirchow describes a 
very remarkable tumor. It grew rapidly in a man, aged twenty- 
two, of good constitution and physical development. The right 
pleural cavity was nearly filled with a solid growth. There were 
similar growths, of smaller size, on the left rib, in the liver, spleen, 
and kidneys. The mediastinal tumor consisted of two portions, a 
larger and a smaller. The larger portion consisted of solid tissue, in 
which were a few cavities. It was very vascular. Part of it was 
composed of dense fibrous tissue. The greater portion, however, 
consisted of loose connective-tissue fibres, of fusiform cells, and of 
large, many-nucleated cells. Some of the fusiform cells were small 
and of the usual appearance, but many were large and presented 
striations like those of young voluntary muscle. The smaller portion 
of the tumor looked like a multilocular cystoid. The cysts varied 
much in size and contained serum, colloid matter, and blood. Some 
of the cysts contained a thick, white material, in which were hairs, 

- — - - • 

1 Consult Hare, "Tumors of the Mediastinum," Philadelphia, 1889. 



THE RESPIRATORY SYSTEM. 391 

•epidermis scales, ciliated epithelium, and cliolesterin. In the fibrous 
tissue about these cysts were pieces of hyalin cartilage. ISTear the 
surface of the tumor the tissue consisted of a fibro-cellular stroma 
forming alveoli filled with epithelium. The tumor on the third left 
rib consisted of connective-tissue fibres and cells, muscle cells, cysts, 
alveoli filled with epithelium, and a small portion of tissue resem- 
bling foetal lung. 



THE TASCULAE SYSTEM. 



THE PERICAEDIUM. 



INJURIES. 

The pericardium may be wounded by penetrating weapons, by 
gunshot wounds, and by fragments of bone. It may be ruptured 
by severe contusions of the thorax, and by rapid extravasation of 
blood into the pericardial sac. 

Perforations -may be produced by empyema, by mediastinal ab- 
scesses, by abscesses of the chest wall and of the liver, by aneurisms 
of the aorta, and by suppurative inflammation of the pericardium. 

DROPSY. 

In most post-mortems we find a little serum, from one-half ounce to 
one ounce, in the pericardial sac. This serum is usually clear and of 
a light-yellow color ; if decomposition has commenced it may be of a 
reddish color, or it may be slightly turbid from the f alling-off of the 
pericardial epithelium. 

Large accumulations of serum are found as part of general drop- 
sy from heart disease, kidney disease, etc. The serum is clear and 
of a light -yellow color. Hydro-pericardium is usually moderate in 
comparison with the accumulations of serum in the other serous cav- 
ities ; sometimes, however, there is a very larg^ amount of serum, 
which hinders the movements and interferes with the nourishment of 
the heart. 

HEMORRHAGE. 

Extravasations of blood in the cavity of the pericardium are pro- 
duced by wounds and rupture of the heart, rupture of the aorta and 
of aneurisms, and occur with pericarditis. Small extravasations in 
the substance of the pericardium are found with scurvy, purpura, 
fevers, etc. 

PNEUMONATOSIS. 

Air or gas in the pericardium is sometimes found as a post-mor- 



OQ 



THE VASCULAR SYSTEM. 39." 

tem appearance, accompanied with drying of portions of the pericar- 
dium. 

Wounds or paracentesis of the pericardium ; the perforation of 
ulcers of the stomach, cavities of the lungs, and ulcers of the oeso- 
phagus, may admit air into the pericardial cavity. In purulent peri- 
carditis with foul, decomposing exudation, gases may be evolved. 

INFLAMMATION. 

Pericarditis is very rarely a primary lesion. It is most frequently 
associated with rheumatism and Bright's disease, but is also found 
with pneumonia, pleurisy, phthisis, endocarditis, pyaemia, and may 
be produced by injuries. 

The inflammations of the pericardium resemble those of the 
pleura. They usually begin acutely or subacutely, but may be- 
come chronic. There is a greater disposition to the escape of blood 
from the vessels than in pleurisy, so that the inflammatory products 
are often mixed with blood. The inflammatory process usually be- 
gins at the base of the heart and from there extends over the rest of 
the pericardium. 

Exudative Pericarditis, 

We may distinguish : 

1. Pericarditis tvith the Production of Fibrin. — In the milder 
examples of this form of pericarditis the pericardium is congested, or 
also studded with minute haemorrhages ; its surface is roughened by 
the deposition of a thin layer of fibrin. In the more severe cases the 
entire surface of the pericardium is covered with a thick layer of 
fibrin, and there are fibrinous adhesions between the visceral and 
parietal pericardium. If the inflammation continues for any length 
of time the pericardium itself becomes thickened and infiltrated with 
cells, and the v/all of the heart may also undergo inflammatory 
changes. 

If the patient recovers the fibrin may be absorbed and the pericar- 
dium return to its normal condition. Or, instead of this, as the fib- 
rin disappears there is a growth of new connective tissue which 
forms permanent thickenings and adhesions of the pericardium, 
which may afterward become calcified. 

2. Pericarditis tvith the Production of Fibrin and a good deal 
of Serum. — In these cases the pericardium is coated with fibrin, but, 
in addition, there is a large efi:usion of serum into the pericardial sac. 
Hiis scrum accumulates at first between the floor of the pericardium 
and the lower surface of the heart, and, as it increases, distends the 
pi^ricardial sac in all directions, })ushing the heart upward ami for- 
ward, llio pericardial sac may be so much distended as io compress 

35 



394 THE VASCULAR SYSTEM. 

the trachea, the left bronchus, the oesophagus, or the aorta. If the 
patients recover the serum is absorbed, and permanent adhesions and 
thickenings are left. 

3. Pericarditis with the Production of Fibrin, Serum, and a 
good deal of Pus. — This variety may have the purulent character 
from the outset, or it may begin as one of the forms just described 
and afterward assume the purulent character. These latter cases 
are apt to run a chronic course. 

In the chronic cases the pericardial sac contains a large amount 
of purulent serum. The pericardium is coated with fibrin and is 
itself thickened and infiltrated with cells. The walls of the heart 
may be the seat of interstitial myocarditis. In some cases the pro- 
ducts of inflammation undergo putrefactive changes ; in some cases 
the serum is absorbed and the fibrin and pus undergo cheesy degene- 
ration ; in some cases extensive connective-tissue adhesions and cal- 
cific plates are formed. 

The pathogenic bacteria most frequently found in the above va- 
rieties of pericarditis are the Streptococcus and Staphylococcus pyo- 
genes and the Diplococcus pneumoniae. 

4. Tubercular Pericarditis. — This lesion may occur b}^ itself, 
but is apt to be associated with tubercular inflammation in the 
vicinity of the heart. There may be miliary tubercles scattered dif- 
fusely, or limited to certain regions in the pericardium, which is 
otherwise little changed. Not infrequently, however, there is a con- 
siderable thickening of the pericardium, either visceral or parietal, or 
both. 

In such cases the new-formed tissue consists of fibrous tissue and 
of tubercle tissue which has undergone extensive cheesy degenera- 
tion. The thickened visceral and parietal pericardium are often 
more or less grown together, so that the pericardial sac may be par- 
tially or almost completely obliterated. A simple inflammatory exu- 
dation of varying form often accompanies the tubercular process. 

TUMORS. 

Fibromata sometimes are developed in the pericardium. They 
are often of polypoid form, and from atrophy of the pedicle may be- 
come free in the pericardial sac. 

Sarcomata and carcinomata occur as secondary growths either 
from continuous infiltration or as metastatic tumors. 

Cysts of the visceral pericardium have been described. 

We have seen a pedunculated cyst, containing about 6 c.c. of 
clear fluid, hanging into the pericardial sac from its attachment near 
the pulmonary artery. The origin of these cysts is obscure. 

Endothelioma. — There may be a growth of flat cells arranged in 



THE VASCULAR SYSTEM. 395 

anastomosing tubules which look like lymphatics, in the pericar- 
dium, resembling similar growths in the pleura 



THE HEART. 
MALFORMATIONS, 

The malformations of the heart are usually closely connected 
with malformations of the aorta and pulmonary artery. They de- 
pend on arrest of, or abnormal, development; on endocarditis, myo- 
carditis, thrombosis, or mechanical causes. 

I. The common arterial trunk is only partially, or not at all, 
separated into aorta and pulmonary artery. The divisions between 
the heart cavities are at the same time defective : 

1. There is one ventricle and no auricle. 

2. There is one ventricle and one auricle. 

3. There is one ventricle and two auricles ; the aorta is alone or 
incompletely separated from the pulmonary artery. 

II. The trunk of the pulmonary artery or of the aorta is ste- 
nosed or obliterated, and from the obstruction to the current of blood 
the development of the septa between the heart cavities is pre- 
vented. 

1. The aorta, at its origin, or in the ascending portion of the 
arch, is stenosed or closed. The pulmonary artery gives off the de- 
scending aorta, and supplies the carotids and subclavians. The fora- 
men ovale remains ojDen, or there is no septum between the auricles. 
The ventricular septum is also usually defective. The right ven- 
tricle is hypertrophied. 

2, The pulmonary artery is stenosed or closed. Its branches are 
supplied by the aorta, through the ductus arteriosus. The ventricu- 
lar septum is defective, the foramen ovale is open, or the auricular 
septum defective. 

III. The malformation affects the aorta and pulmonary arter}* 
after they are more fully developed. 

1. There is stenosis of the aorta between the left subcla^4an and 
ductus arteriosus, or just at the opening of the ductus arteriosus. 
The descending aorta is then a continuation of the pulmonary 
artery. 

2. The aorta gives off all its branches from the arch, but the de- 
scending aorta is a continuation of the pulmonary artery : or tht^ 
carotids may spring from the aorta, the subchivians from the pul- 
monary artery. 

3. The vessels are transposed ; the pulniv)nary artery arises from 
the left, the aorta, from the right ventricle : the pulmonary veins 



396 THE VASCULAR SYSTEM. 

empty into the left, the vense cavse into the right auricle ; or the 
veins also may be transposed. The septa are defective. 

IV. The aorta and pulmonary artery are normal, but the cardiac 
septa are defective. 

1. The foramen ovale remains partly open. This condition may 
continue through life without giving an;^" trouble. 

2. The ductus arteriosus may remain open for many years ; this 
also may cause no disturbance. 

3. There is a small or large opening in the ventricular septum. 
This may give rise to no symptoms, unless disease of the heart or 
lungs be superadded. 

V. Either of the auriculo-ventricular orifices may be entirely 
closed. The foramen ovale remains open, and the ventricular sep- 
tum is defective. 

VI. The valves of the different orifices of the heart may be ab- 
sent or defective. The arteries or the ventricles are usually defec- 
tive at the same time. 

The aortic and pulmonary valves may consist of two large or 
four small leaves, instead of the usual three. The edges of the 
semilunar valves ma}^ be fenestrated. These alterations are usually 
of no significance. 

Generally speaking, the existence of openings between the two 
auricles or the two ventricles, admitting some admixture of venous 
and arterial blood, produces no marked change in the circulation. 
If, however, the passage of the current of venous blood into the 
right heart is in any way interfered with, the consequences are very 
serious. Cyanosis is produced, the skin is of a bluish color, the 
small veins and capillaries are dilated, exudation of serum and 
hj^pertrophy of connective tissue take place, especially in the fingers 
and toes. 

Besides the malformations already mentioned we may find : 

Entire absence of the heart. 

Abnormal septa and chordae tendineas in the heart cavities. 

Abnormal shapes of the heart. 

Abnormal positions of the heart. 

(a) There is a smaller or larger defect in the walls of the thorax, 
so that the heart projects on the outside of the chest ; the pericar- 
dium is usually absent. 

(6) The diaphragm is absent, and the heart is in the abdominal 
cavity. 

(c) The heart is in some part of the neck or head ; this occurs 
only in fcetuses very much malformed. 

(d) The heart is transposed, being on the right side. 



THE VASCULAR SYSTEM. 397 

ABNORMAL SIZE OF THE HEART. 

(a) The heart may be abnormally large in connection with ob- 
structive anomalies of the great vessels. 

(b) The heart may be abnormally small (hypoplasia). This most 
frequently occurs, according to Virchow, in chlorotic individuals and 
those who are the victims of the hsemorrhagic diathesis. In these 
cases the aorta and other large arteries are apt to be unusually small 
and thin-walled. 

Very rarely two more or less perfect hearts are found in the same 
thorax. 

CHANGES IN POSITION. 

Changes in the position of the heart are congenital or acquired. 
The congenital malpositions have already been mentioned. 
The acquired malpositions are caused by : 

1. Hypertrophy of the heart ; its long axis approaches the hori- 
zontal direction. 

2. Changes in the thoracic viscera. Emphysema of both lungs 
pushes the heart downward. Emphysema, pleurisy with effusion, 
or pneumothorax of one side pushes the heart to the other side. 
Pleurisy or chronic pneumonia, producing retraction of one side of 
the thorax, draws the heart to that side. E^ew growths, aneurisms, 
and curvatures of the spine displace the heart in various directions. 

3. Changes in the abdomen. Accumulations of fluid and new 
growths in the abdomen, and tympanites, may push the heart up- 
ward. 

WOUNDS AND RUPTURES. 

Wounds of the heart are produced by penetrating instruments, 
by bullets, and by fragments of bone. The right ventricle is the 
more frequently wounded ; next the left ; rarely the auricles. 

The wound may penetrate into the cavities of the heart or only 
pass partly through its wall, or a bullet or the broken end of a weapon 
may be embedded in the wall. If the wound penetrates into a cavity 
and is gaping, death follows instantly and the pericardium is found 
filled with blood. If the wound be small and oblique, the blood may 
escape gradually and death may not ensue for several days. In rare 
cases adhesions are formed with the pericardium and the wound 
cicatrizes. Wounds which do not penetrate may cause death by the 
inflammation which they excite, or may cicatrize. 

Bullets and foreign bodies may become encapsulated in the heart 
wall and remain so for j^ears. 

Eiipfures of the heart wall occur in various ways : 

1. Sevej'e contusions of the thorax may produce rupture, usually 
of one of the auricles. 



398 THE VASCULAR SYSTEM. 

2. Spontaneous rupture occurs usually in advanced life. Rupture 
is most frequent in the left ventricle, and, in a considerable proportion 
of cases, near the apex. There is usually one rupture, but sometimes 
more. The rupture is usually oblique and larger internally than ex- 
ternally. The heart wall, near the seat of rupture, may be infiltrated 
with blood, or blood may infiltrate the subDericardial fat. The heart 
wall may be of normal thickness, or thin ; it is usually soft and in a 
condition of fatty infiltration or degeneration. The rupture very 
frequently takes place when the patient is quiet. Death may be 
almost instantaneous or may not ensue for several hours. 

Fatty degeneration leading to rupture of the heart may be gene- 
ral, or it is frequently circumscribed and due to obliterating endar- 
teritis, atheroma, thrombosis, or embolus of one of the coronary 
arteries, whereby a portion of the heart wall is deprived of nourish- 
ment and degenerates. Or rupture of a branch of one of the coronary 
arteries may induce rupture of the heart wall. Acute and chronic 
myocarditis, with or without the formation of abscess or cardiac 
aneurism, or the presence of tumors in the heart wall, or hydatids, 
may lead to the rupture. 

3. In very rare cases rupture is produced by stenosis of the aorta 
and dilatation of the heart cavities. 

4. Rupture of the papillary muscles and tendons may be produced 
by fatty degeneration or inflammatory or ulcerative processes. 

ATROPHY. 

Atrophy of the walls of the heart may be accompanied with no 
change in the size of its cavities ; or with dilatation (the same as pas- 
sive dilatation); or, more frequently, with diminution in the size of 
the cavities. 

The atrophy involves most frequently all the cavities of the hearty 
but may be confined to one or more of them. 

The muscular tissue appears normal, or brown from the presence 
of little granules of pigment in the muscular fibres, which are some- 
times present in large numbers — brown atrophy ; or the muscular 
fibres may undergo fatty degeneration ; or there may be an abnor- 
mal accumulation of fat beneath the pericardium ; or there may be 
a peculiar gelatinous material beneath the pericardium — this con- 
sists of fat which has undergone mucous degeneration. The heart 
may be so much atrophied as to weigh four ounces. 

The causes of atrophy of the heart are : 

1. It is a congenital malformation; the heart of an adult then 
looks like that of an infant. 

2. Any chronic and exhausting disease, repeated hsemorrhages, 
old age, typhus fever, dysentery, etc. , may produce atrophy. 



THE VASCULAR SYSTEM. 309 

3. Chronic pericarditis, with large serous effusion, or with thick- 
ening of the pericardium, producing constriction of the coronary ar- 
teries. 

4. Stenosis, atheroma, calcification, or thromlxjsis of the coronary 
arteries may produce partial or total atrophy. 

5. Myocarditis, with fatty or fibrous degeneration. 

6. Mitral stenosis may cause atrophy of the left ventricle. 

HYPERTROPHY. 

All the cavities of the heart may have their walls hypertrophied, 
or the thickening may involve one or more.' While the wall of a 
ventricle is thickened, its cavity may retain its normal size — simple 
hypertrophy; or be dilated — eccenti'ic hypei^trophy j or it maybe 
contracted — coiiceiitric hypertrophy. 

Care should always be exercised in judging of this condition, for 
a firmly contracted heart seems to have a small cavity and thick 
walls. The existence of such a condition as concentric hypertrophy 
is denied by some authors. Eccentric hypertrophy is the most com- 
mon form. Simple hypertrophy is not common, but may occur in 
connection with the atrophied kidneys of chronic diffuse nephritis. 
The muscle tissue in hypertrophied hearts is firmer and denser than 
normal, and is apt to have a darker color. Fatty degeneration may. 
however, be associated with it, giving the walls a lighter appear- 
ance. It is probable that the increase of tissue in the hypertrophied 
heart wall is the result of increase both in size and number of the 
nuiscle fibres. 

Hypertrophy of both ventricles increases both the length and 
breadth of the heart. Hypertrophy of the left ventricle (alone) in- 
creases its length. The apex is then lower and further to the left 
than usual. Hypertrophy of the right ventricle (alone) increases 
the breadth of the heart toward the right side ; but sometimes the 
right edge of the heart retains its normal situation and the apex is 
displaced to the left. With large hypertrophy of both ventricles, 
the base of the heart may sink, so that its long axis approaches a 
horizontal direction. 

Hypertrophied hearts may weigh from forty to fifty ounces, or 
even more. 

Hypertrophy of the heart may depend upon a variety of causes : 

1. Changes in the valves ; either insufficiency or stenosis in the 
valves leading from a cavity, and insufficiency in valves leading to a 
cavity, may induce hypertrophy of its walls. 

2. Obstruction to the passage of blood through the arterial sys- 
tem, as in atheroma and other diseases of the intiina : congouital or 
acquired stenosis of vessels, pressure of tumors, etc., tni vessels : 



400 THE VASCULAR SYSTEM. 

certain forms of chronic diffuse nephritis, especially atrophied kid- 
neys, lead to hypertrophy of the left ventricle, and sometimes sec- 
ondarily to hypertrophy of the right ventricle. 

3. Obstruction to the passage of blood through the pulmonarj^ 
artery by stenosis or by certain diseases of the lungs, particularly 
emphysema and chronic phthisis, may lead to hypertrophy of the 
right ventricle, and, secondarily, of the right auricle and left ven- 
tricle. 

4. Any cause, whether muscular or nervous, which increases the 
rapidity and force of the heart's contractions, may produce hyper- 
trophy. 

5. Dilatation of the ventricles, from any cause, is frequently fol- 
lowed by hypertrophy. 

6. Pericarditis may produce hypertrophy by inducing softening* 
and dilatation of the ventricles, or by lea^^ng adhesions which ob- 
struct the hearths action. Chronic mvocarditis also may lead to hv- 
pertrophy. 

Finally, for some cases of h^^pertrophy no satisfactory cause can 
be found. 

It should be borne in mind that an increase in the amount of fat 
in and about the heart may make the organ appear larger, w^hen 
there may be actually a considerable decrease in the amount of mus- 
cle tissue. 

DILATATION. 

Dilatation may be combined with hypertrophy — active dilata- 
tion ; or there may be no increase of muscle tissue, but a thinning 
of the walls proportionate to the dilatation of the ca\dty — passive 
dilatation. 

Either one or all of the heart cavities may be dilated, the au- 
ricles most frequently ; next the right ventricle ; least often the left 
ventricle. 

Active dilatation has been considered under hypertrophy. 

Passive dilatation may be produced by : 

1. Changes in the valves. Mitral or aortic stenosis or insuf- 
ficiency may produce dilatation of the auricles and right ventricle. 
Pulmonary stenosis or insufficiency may produce dilatation of the 
right auricle and right ventricle. Aortic insufficiency, with or 
without stenosis or mitral insufficiency, may produce dilatation of 
the left ventricle. Dilatations from these causes are often succeeded 
and compensated for by hypertrophy of the heart walls. 

2. Changes in the muscular tissue of the heart walls. Serous 
infiltration from pericarditis, myocarditis, fatty degeneration and in- 
filtration, atrophy of the muscle fibres, may all lead to dilatation. 



THE VASCULAR SYSTEM. -iOl 

3. A beaii; which is already hypertrophied may, from degenera- 
tion of the muscle, become dilated. 

4. Acute exudative inflammations of the lungs and acute pleuritic 
exudations, by rendering a large number of vessels suddenly im- 
permeable to the blood current, may produce sudden stasis in the 
pulmonary artery and dilatation of the right heart. 

5. There are curious cases of acute and chronic dilatation of the 
ventricles for which no mechanical cause can be found and which 
are very fatal. 

DEGENERATIONS. 

Acute Degeneration ; Parenchymatous Degeneration of the 
Heart Muscle. — This lesion frequently occurs in typhoid and typhus 
fever, pyaemia, erysipelas, and other infectious diseases, as well as 
in the exanthemata, as a result of burns, and under a variety of 
other conditions. It is characterized by the presence in the muscle 




Fig. 207.— Fattt Degeneration of the Heart Muscle. Teased. 

fibres of the heart of greater or less numbers of albuminous gran- 
ules of various sizes, most of them very small. They are not as re- 
f ractile as fat droplets, and are insoluble in ether, Avhile swelling up 
and becoming almost invisible under the influence of acetic acid. 
Sometimes they are so abundant as to conceal the striations of the 
fibres. The degeneration is usually quite uniformly diffused through 
the heart, whose walls are softer than normal and of a gra^-ish 
color. This lesion may be associated with or followed by fatty de- 
generation. 

Fattij Regeneration of the Heart Muscle. — This consists in the 
transformation of portions of the muscle fibres of the heart into fat, 
which collects in the fibres in larger and smaller droplets, sometimes 
few in number, sometimes so abundant as to outiroly destroy or 
conceal the normal striations (Fig. '-207). These droplets are sohibU^ 
in ether, and remain unchanged on treatment with acetic acid. 
This degeneration is sometimes quite univtM-sal, but is more apt tv^ 
occur in patches, giving the heart muscle a mottled appearance. 
This mottling may usually bi^ best seen 0!i the }iapillarv muscles. 
36 



402 



THE VASCULAR SYSTEM. 



The degenerated areas have a pale-yellowish color, and the muscle 
tissue is soft and flabby ; but when moderate or slight in degree the 
gross appearance may be little changed, and the microscopical ex- 
amination be necessary for its determination. This degeneration 
may lead to thinning of the walls, or to rupture of the heart, or to 
inability to fulfil its functions. It is not infrequently the cause of 
sudden death. 

It may be secondary to hypertrophy of the heart, to inflamma- 
tion of the heart muscle, or to pericarditis ; to disturbances of the 
circulation in the coronary arteries by inflammation, atheroma, etc. 
It may be due to deteriorated conditions of the blood in wasting dis- 
eases, excessive haemorrhages, exhausting fevers, leukaemia, etc., 




Fig. 203.— Fatty Infiltration or Lipomatosis op the Heart. 

The lesion is excessive, the heart muscle being to a larg^e extent atrophied. (The fat cells are 
represented in the drawing, for the salie of clearness, of relatively too large size.) 



or to poisoning with phosj^horus and arsenic. It may occur in other- 
wise apparently healthy persons. 

Fatty Degeneration of the Endocardium. — It is not uncom- 
mon to find, especially in elderly persons, fatty degenerations occur- 
ring in patches, especially on the valves, but also on the general 
endocardium. They may also occur in ill nourished and anaemic 
individuals. Small, or even considerable, areas of fatty degenera- 
tion appear, as a rule, to be of little or no clinical significance. They 
are at least not inconsistent with perfect health. In these areas 
of fatty degeneration the connective-tissue cells are more or less 
completely filled with larger and smaller fat droplets. 

Annjloid Degeneration of the endocardium or the walls of the 



THE VASCULAR SYSTEM. 



urd 



blood vessels and intermuscular connective-tissue septa is a not very 
infrequent, but usually not very important lesion. 

Hyalin Degeneration sometimes occurs. 

Calcification of the products of inflammation in pericarditis, or 
of connective-tissue membranes in chronic pericarditis, sometimes 
occurs, and in the latter case the heart may be more or less enclosed 
by a calcareous shell. . The muscle fibres of the heart wall may, 
though rarely, become densely infiltrated wit.h salts of lime. 

Fatty Infiltration or Lipomatosis of the Heart. — This lesion, 
which should be clearly distinguished from fatty degeneration, con- 
sists of an unusual accumulation of fat about the heart and between 
its muscle fibres (Fig. 208). 

The subpericardial fat, which may be present in considerable quan- 




FiG. 209 —Atrophic Pericardial. Fat. 

From young person dead of carcinoma of the stomach and peritoneum. Stained with osmic 
acid and teased. 



tity under normal conditions, may be so greatly increased in amount 
as to form a thick envelope enclosing nearly the entire organ. Some- 
times the accumulation of fat extends into the walls of the heart, 
between the muscles, causing atrophy of the latter, frequently to a 
very great extent, so that the function of the heart is seriously in- 
terfered with. This occurs sometimes in general obesity, or as a re- 
sult of chronic pericarditis, or in drunkards, or in debilitated or old 
persons. 

Atrophy of the pericardial fat f/55?/(^ not infrequently occurs in 
persons emaciated by chronic disease, and then the usual situations 
of the fat are occupitnl by a tissue resembling nuirous tissue in its 
gross characters. Microscopical exainination shcnvs that in thi< 
atrophic fat the fat cells have largely lost tlieir contents, and \\\o 



404 THE VASCULAR SYSTEM. 

whole tissue has undergone a partial reversion to its original embry- 
onic form (see Fig. 209). 

Myomalacia. — When, through obliterating endarteritis, athero- 
ma, thrombosis, or embolus of a branch of the coronary arteries, 
the blood supply is cut off from a circumscribed portion of the heart 
wall, the tissue in the affected area may undergo fatty degeneration, 
leading to rupture. Or, instead of extensive fatty degeneration, the 
muscle fibres may break down into a granular detritus and the con- 
nective tissue about them suffer retrograde metamorphosis, so that 
the whole affected area may be soft and yelloAvish-white or grayish 
in color. If, as not infrequently occurs, there is considerable extra- 
vasation of blood, the degenerated area may be of a dark-red color. 
Under these conditions the wall may rupture ; or acute inflammatory 
processes may occur ; or the degenerated tissue may be gradually 
absorbed, and replaced by new connective tissue which gradually 
grows dense, shrinks, and assumes the characters of cicatricial tis- 
sue. This may occur in any part of the heart wall or in the paj)il- 
lary muscles. When the heart wall is involved the new-formed 
connective tissue may }T.eld to the blood pressure from within and 
an aneurism of the heart be formed. 

Fragmentation of the Myocardium. — Attention has been called 
Ijy a number of observers to a condition of the heart muscle some- 
times observed, it is said, in acute infectious diseases, in acute and 
chronic diseases of the central nervous system, and in sudden death 
from a variety of causes. The muscle tissue is soft, friable, opaque, 
and often yellowish. Examination shows a loosening of the muscle 
cells from one another, as if by some change in the cement sub- 
stance. ^ It is still questionable whether this may not be a post-mor- 
tem change. 

IXFLAMMATIOX. 

Endocarditis. 

The endocardium is a connective-tissue membrane which lines 
the cavities of the heart and forms its valves. Its inner surface is 
covered with a layer of endotheUal cells. It is but poorly supplied 
"^vith vessels, and the inflammations which attack it are of the cel- 
lular variety. The ordinary products of inflammation, pus, fibrin, 
and serum, are scanty or absent altogether. The connective-tissue 
cells and basement substance are principally concerned in the inflam- 
matory processes. The new tissue thus produced is prone to de- 
generation and calcification. The roughening of the endocardium 

1 Tedeschi, Vircliow's Archiv, Bd. cxxviii., Heft ii., p, 185, 1892 — literature and 
experiments. 



THE VASCULAR SYSTEM. 405 

due to the inflammation often causes a coagulation of fibrin on the 
inflamed surface. 

In foetal life it is the endocardium of the right heart, in extra- 
uterine life that of the left heart, which is usually inflamed. 

The endocardium which forms the valves is that which is most 
frequently inflamed, but the other portions of it are by no means 
exempt. 

1. Simple Acute Endocarditis. — This is most apt to occur in 
connection with rheumatism, but may occur under other conditions. 
It may attack a heart which was previously healthy, or one in 
which the lesions of chronic endocarditis already exist. 

In some cases the only lesion is a simple swelling of the A^alves. 




Fig. 210. -^Vegetation on Aortic Valve in Endocarditis. 
Showing granular thrombus over the surface. 

They are thick and succulent, but their surfaces remain smooth. 
The basement substance is swollen, and there is a moderate pro- 
duction of new connective-tissue cells. 

In other cases the growth of connective-tissue cells is very much 
more marked, the basement substance is split up, and little cellular 
fungous masses, called vegetations, project from the free surface of 
the endocardium. On these rou^'hened surfaces the fibrin of the 
blood is deposited, and so vegetations of considerable size may bo 
formed (see Fig. 210). 

In still other cases the cell growth, while in some places it forms 
vegetations, in other places degenerates, and thus portions of tho 
valves are destroyed. This is simple acute ulcerattre endocar- 
ditis. 



406 



THE VASCULAR SYSTEM. 



In some cases of this disease the patients recover and the valves 
seem to return to a normal condition ; in other cases the valves are 
left permanently damaged ; and in still others chronic endocarditis 
follows the acute form. 

2. Mycotic or Malignant Endocarditis (malignant ulcerative 
endocarditis). 

The direct inciting cause of simple acute endocarditis of the forms 
described above is unknown. But in a considerable number of cases 
of acute endocarditis bacteria have been found in and about the 
vegetations (see Fig. 211), and proved, by careful experiments, to 
stand in a causative relation to the lesion. 

Those cases of acute endocarditis in which the lesions are in- 
duced by the direct action of bacteria are called mycotic or malig- 
nant endocarditis J or, since the new-formed as well as the old 
tissue about the bacteria is apt to become necrotic and thus lead to 




Fig. 211.— Mycotic E>rDocARDiTis. 
Section of vegetation, showing colonies of micrococci stained with methyl violet. 



larger or smaller losses of substance, the lesion is often called ulcera- 
tive endocarditis. 

Cultivations of the bacteria occurring in the heart lesions in ma- 
lignant endocarditis have shown that, while various species of 
bacteria may occasionally act as an inciting cause, it is most com- 
monly induced by the Staphylococcus pyogenes aureus, the Strepto- 
coccus pyogenes, and the Diplococcus pneumonicie. 

It has been, furthermore, found that a lesion or injury of the en- 
docardium, either on the heart valves or elsewhere, predisposes to 
the lodgment and groAvth upon them of the disease-producing 
bacteria when once they have gained access to the circulating blood. ' 

^ For a detailed consideration of the relationship of bacteria to malignant endo- 
carditis, with experiments and literature, see Prudden, Am. Jour. Med. Sciences, 
January, 1S87 ; Weichselbaum, Ziegler's Beitrage zur path. Anat., Bd. i v., 1888, 
p. 127. 



THE VASCUl^AR SYSTEM. 



40? 



Mycotic endocarditis is frequently a secondary complicating le- 
sion, but may occur as a primary disease. It is most apt to be asso- 
ciated with the acute infectious diseases, and in many cases may be 
regarded as one of the local manifestations of pysemia. 

In some cases there is a formation of new tissue in the form of 
organized vegetations on the valves or general endocardium ; in 
other cases necrosis either of the new-formed or the old tissue is the 




Fig. 212.— Chronic Endocarditis. 
Showing " vegetation " on heart valve with large blood clot— miti-al valve. 



most marked feature. Blood clots are apt to form on the aft'ected 
surfaces and often largely make up the so-called vegetations. Tht^ 
mitral and aortic valves are frecxuently the seat of the lesiini. but it 
may occur elsewhere. 

Detachment of bacteria containing fragments of the vegetations 
or clots may give rise to single or multiple infectious oiuboU (see j). 
()1) and abscesses in variousparts of the body, such as thespUvn. kid- 



408 



THE VASCULAR SYSTEM. 



neys, brain, skin, heart wall, etc. Bacteria similar to those in the 
heart lesion may be found in these secondary abscesses (see Fig. 
49). 

It is probable that these abscesses in ulcerative endocarditis do 
not always arise from cardiac emboli, but may precede the heart 
lesion. 

3. Chronic Endocarditis may succeed acute endocarditis, or the 
inflammation may be chronic from the outset. It affects most fre- 
quently the aortic and mitral valves, and the endocardium of the left 
auricle and ventricle ; similar changes in the right side of the heart 
being much less frequent. 



x 





Fig. 213.— Chboxic Eitdocarditis. 
Showing "vegetation " — aortic valve. 



There are two main anatomical varieties of chronic endocarditis, 
which may occur separately or together. 

(1) The endocardium is thick and dense, its surfaces are smooth 
or covered with small, hard vegetations or ridges ; it is often infil- 
trated vdth the salts of lime. 

(2) There is a growth of connective-tissue cells in the endocar- 
dium, ^vith a splitting-up of the basement substance. Some of the 
new cells continue to Uve, others degenerate. By the combination 
of such a cell growth and destruction the endocardium is in some 
23laces destroyed, in others changed into projecting vegetations. 
Fibrin is deposited on the roughened surfaces (Figs. 212 and 213). 
After a time the condition may be further comphcated by the 
shrinkage and deposition of the salts of lime in the neiv tissue and 



THE VASCULAR SYSTEM. 409 

in the endocardium. All these changes may extend to the wall of 
the heart beneath the endocardium. 

The most important result of chronic endocarditis is its effect on 
the heart valves, producing insufficiency and stenosis. The changes 
in the valves are followed by changes in the walls and cavities of the 
heart, and disturbances of the circulation throughout the body. 

4. Chronic Ulcerative Endocarditis. — Large ulcers or perfora- 
tions of the valves may be formed in chronic endocarditis, upon 
which clots may form, so that in gross appearance a great similarity 
exists between this and malignant ulcerative endocarditis, particu- 
larly if the latter have been engrafted upon an already chronically 
diseased endocardium. The microscopical and biological examina- 
tions must usually be resorted to in order to determine the exact sig- 
nificance of the lesion. 

5. Tubercular Endocarditis may occur in connection with tu- 
bercular pericarditis or general miliary tuberculosis. The tubercles 
may be small and single, or grouped in masses, and show the usual 
degenerative changes. 

Myocarditis. 

The inflammatory changes in the walls of the heart involve pri- 
marily the interstitial tissue and blood vessels, the muscle fibres 
being secondarily affected by atrophic and degenerative changes. 

Interstitial Myocarditis may be acute and purulent, or chronic 
with the formation of new connective tissue. 

Acute Purulent Myocarditis may be diffuse, infiltrating the 
wall of the heart with pus. This may occur as a complication of 
scarlatina and from unknown causes. 

More frequently the purulent inflammation is circumscribed, pro- 
ducing abscesses. These occur with pyaemia, mycotic ulcerative en- 
docarditis, and other infectious diseases. They are of different 
sizes and either single or multiple. They are produced by the lodg- 
ment of infectious emboli in small vessels. The contents of the ab- 
scesses consist of pus, broken-down muscle tissue, and bacteria. 
These abscesses may open into the pericardial sac and set up a pu- 
rulent pericarditis ; or into a heart cavity, giving rise to thrombi in 
the heart and emboli in different parts of the body : or the wall of 
the heart is weakened b}" the abscess so that it ruptures, or an aneu- 
rismal sac is formed ; or an abscess in the interventricular septuni 
may establish an opening between the ventricles ; or the suppura- 
tive process may extend upward and form an abscess in the connec- 
tive tissue at the base of the heart. 

In rare cases the patients recover, th(^ contents of the abscesses 
become dry and hard, and enclosed by a. wall of tibrous tissue. 
37 



410 THE VASCULAR SYSTEM. 

Chronic Interstitial Myocarditis may be secondary to pericar- 
ditis or endocarditis; to obliterating endarteritis of the branches of 
the coronary artery, myomalacia, or may occur by itself. There is a 
growth of new connective tissue or of granulation tissue between the 
muscular fibres, with atrophy and degeneration of the muscle. This 
growth may be in the form of circumscribed patches (Fig. 214), or 
diffused over a considerable part of the wall of the heart. Such an 
interstitial inflammation is often followed by dilatation of the cavi- 
ties of the heart, by the formation of aneurisms of the wall of the 
heart, and of thrombi in the cavities of the heart. 

Syphilitic Myocarditis is accompanied by the growth of con- 
nective tissue or granulation tissue in the wall of the heart between 
the muscular fibres. The pericardium and endocardium may also be 









1 . 






^t^V, ^- I'll / .,®-^i,'9s::^^ ^ |#L'^^ «e^^ ,^^^„ 



Fig. 214.— Chronic Interstitial Myocarditis. 
Showing transverse section of a portion of a papillary muscle. 

thickened, and pericardial adhesions may be formed. Gummata of 
the heart are of rare occurrence. 

CHANGES IN THE VALVES. 

Fenestration of the valves is usually a change productive of no 
bad consequences. It occurs very frequently in the aortic and pul- 
monary valves. The valves may be thinner than usual, and close 
to their free edges are small slits extending from the centre to the 
attached edges of a leaf. 

Aneurisms of the valves are produced in two ways : 

1. They are the result of endocarditis. One of the lamellae of the 
leaf of a valve is destroyed, and the other lamella is converted into 
a sac filled with blood. These aneurisms are found in the aortic 
valve, projecting into the ventricle ; and in the mitral valve, project- 
ing into the auricle. Not infrequently the wall of the aneurism 
gives way, so that there is a rupture entirely through the valve. 

2. The entire thickness of a leaf of a valve is converted into a 



THE VASCULAR SYSTEM. 411 

sac filled with blood. This occurs in the aortic, mitral, and tricus- 
pid valves ; its cause is unknown. 

Hcemorrhage in the substance of the valves is sometimes found 
in very young children. It does not appear to have much clinical 
importance. 

ANEURISM OF THE HEART. 

Sacs filled with blood, situated in the walls of the heart and com- 
municating with its cavities, are formed in several different ways. 

1. In consequence of inflammatory processes in the endocardium 
and muscular tissue, a small or large portion of the wall is converted 
into fibrous tissue. The portion thus changed no longer resists the 
pressure of the blood from within, and is driven outward. Such a 
pouch may be a circumscribed sac communicating with the heart 
cavity by a small opening, or may look like a dilatation of part of the 
ventricle. The wall of such an aneurism becomes thinner as the sac 
increases in size. It is composed of the endocardium, new fibrous 
tissue, visceral pericardium, and sometimes the adherent parietal 
pericardium. The walls may calcify, or rarely they become so thin 
as to rupture externally or into the right ventricle. The sacs may 
contain fluid blood or be filled up with fibrin. 

Such aneurisms are usually situated in the wall of the left ven- 
tricle ; rarely in that of the left auricle. If they are in the septum 
they may project into the right ventricle. They are usually single, 
but sometimes two or three are found in the same heart. 

2. Fatty degeneration of the heart wall may reach such a point 
that the wall yields and is pouched out into an aneurismal sac. 

3. Endocarditis and myocarditis, or fatty degeneration, may so 
soften a portion of the heart wall that the endocardium and part of 
the muscular tissue are ruptured and a ragged cavity is formed. 
This form of aneurism usually does not attain a large size, but soon 
ruptures externally and causes the death of the patient. 

THROMBOSIS OF THE HEART. 

It is very common to find after deafti, in the heart cavities, yellow, 
succulent, semi-translucent masses. They are most common and of 
firmest texture in persons who die of acute inflammatory diseases. 
They may adhere quite firmly to the walls of the heart, and may ex- 
tend in long, branching cords into the vessels. The}' are formed in 
the last hours of life and just after death. They have no clinical or 
pathological importance. 

Coagulations of the fibrin of the blood in the heart dc>. however, 
•occur during life, and may exist for 3'ears. If the fibrin adlieres to 
the valves in small masses these are called vei^etations : if it coai^u- 



412 THE VASCULAR SYSTEM. 

lates in the heart cavities in larger bodies they are called thrombi or 
heart polypi. 

Such thrombi are found in all the heart cavities. They form flat- 
tened masses firmly adherent to the endocardium ; or rounded bodies 
in the spaces between the trabeculsB; or have a polypoid shape and 
are attached by a narrow pedicle, or are free in the cavity. 

They are usually found in connection with some valvular lesion 
which prevents the free circulation of blood through the heart. 

They are firm, dry, and of a whitish color ; they may soften and 
break down at their centres, so as to look like cysts filled with pus, 
or they may calcify. They are usually entirely unorganized, con- 
sisting simply of fibrin, but may become organized. 

One of us (Delafield) has seen an organized thrombus in the heart 
of a man, whose history was unknown, who was found dead in the 
street. 

Unorganized polypoid or globular and unattached thrombi of the 
auricles are of occasional occurrence. Wilson presented before the 
New York Pathological Society, 1892, a large thrombus of the auricle 
which was partly organized. 

Sometimes sarcomatous and carcinomatous tumors in different 
parts of the body are accompanied by the formation of thrombi in 
the heart cavities which are composed partly of coagulated blood,, 
partly of tissue like that of the primary tumor. 

TUMORS. 

Primary tumors. in the heart are rare, but sarcomata, myxomata, 
fibromata, and lipomata may occur. Rhahdomyomata, probably 
congenital, may occur in the heart wall as circumscribed nodular 
masses. A cavernous tumor of this kind has been described. Sec- 
ondary tumors, as a result of metastasis, or of continuous growth from 
adjacent parts, are not very infrequent. These are usually carcino- 
mata or sarcomata. Secondary chondromata have been observed. 

PARASITES. 

Echinococcus sometimes occurs in the heart wall and may perfo- 
rate into the cavities. Cysticercus cellulosse has been observed. 

THE BLOOD VESSELS. 
ATROPHY AND HYPERTROPHY. 

Atrophy of the blood vessels may involve the entire trunk or 
some of its elements. It may occur as a part of general malnutri- 
tion of the body, or in connection with atrophy of particular organs,, 



THE VASCULAR SYSTEM. 413 

or as an accompaniment of various diseases of the vessels them- 
selves. 

Hypertrophy, which is especially seen in the arteries, may occur 
in the establishment of a collateral circulation upon the closure of 
arterial trunks; or it may occur as the result of increased blood pres- 
sure, as in some forms of hypertrophy of the heart. 

DEGENERATION. 

Fatty Degeneration. — This may occur in the walls of otherwise 
unaltered vessels, or in those which have undergone a variety of in- 
flammatory or degenerative changes. It may occur either in the in- 
tima or media, or both, and may be so extensive as to form a very 
prominent gross lesion, or so little developed as to require the micro- 
scope for its recognition. When marked, especially if occurring in 
the intima of large vessels, smaller and larger spots or stripes or 
patches may be seen, of a yellowish-white color, usually sharply cir- 
cumscribed, and sometimes smooth, sometimes roughened on the 
surface. It is most apt to occur in the aorta, but may be found in 
any of the vessels. In moderate degrees of the lesion w^e find on 
section that the cells of the intima contain fat droplets in greater or 
less number. When further advanced, not only are the cells crowded 
with fat droplets, but the intercellular tissue also may be more or less 
densely infiltrated with them. Sometimes the infiltration is so dense 
that the tissue breaks down, and there may be an erosion of the sur- 
face, forming a so-called fatty ulcer. When the media is involved 
the muscle cells contain fat droplets. It may lead to the formation 
of aneurism or to rupture of the vessels. 

Calcification usually occurs in vessels otherwise diseased, and 
may involve either the intima or media. It consists in the deposi- 
tion of salts of lime either in the cells or intercellular substance. 
The lime may be in the form of larger or smaller granules or in 
dense translucent plates. 

Amyloid Degeneration, which may affect all the coats of the ar- 
teries, but especially the intima and media, will be considered under 
the lesions of the organs in which it most commonly occurs. 

Hyalin Degeneration may cause thickening of the inthna of 
the blood vessels by its conversion into or infiltration with a homoge- 
neous material somewhat similar to amyloid (see page S-t). Or it 
may involve the entire wall of smaller vessels, converting thoni into 
irregular lumpy ccn-ds. The lumen of vessels thus changed may be 
obliterated or occluded bv thrombi. 



414 THE VASCULAR SYSTEM. 

THE ARTERIES. 
INFLAMMATION. 

Acute Arteritis. 

Acute inflammation of the walls of the arteries is, in the major- 
ity of cases, the result of injury, or of an inflammation in the vicin- 
ity of the vessel, or of the lodgment within it of some foreign body 
of an irritating or infectious nature. The inflammatory process may 
be largely confined to the inner layer of the vessels — endarteritis ; 
or it may commence in the outer layers — periarteritis ; or it may 
involve the entire wall. 

The blood vessels in the outer layers may be congested, the tissue 
oedematous and infiltrated with pus cells, and the entire wall may 
become necrotic. The intima, if this layer is involved, loses its natu- 
ral gloss, looks dull and swollen. It may become infiltrated with 
pus from the outer layers, and it may become necrotic. Under these 
conditions thrombi usually form, and in these may occur the various 
changes which have been already described on page 60, 

Chronic Arteritis. 

Since the publication of the studies of Gull and Sutton on arterio- 
capillary fibrosis, attention has been every year more and more di- 
rected to morbid changes in the arteries as one of the most frequent 
of diseased conditions. 

It is evident that these morbid changes are caused by alcohol, 
lead, gout, and syphilis; that the disposition to them is hereditary in 
some families ; that they constitute one of the regular senile changes ; 
that they are often associated with chronic diseases of the viscera ; 
that the patients can be unconscious of their existence, and that, on 
the other hand, they can cause most distressing symptoms, and even 
death. 

At the present time it is customary to speak of these morbid con- 
ditions under the names of arterio-sclerosis and atheroma, and to 
accept the conclusions drawn by Thoma from an extended series of 
studies. Thoma teaches that : 

1. Every long-continued slowing of the blood current causes con- 
traction of the middle coat of the aorta, and, if this is not sufiicient 
to accelerate the blood current, to a growth of connective tissue in the 
intima. 

2. Primary diffuse and nodular arterio-sclerosis depends upon a 
weakening of the wall of the blood vessel due to constitutional con- 
ditions. This is followed by dilatation of the vessel, slowing of the 
blood stream, and then the growth of connective tissue in the intima. 



THE VASCULAR SYSTEM. 



415 



3. Secondary arterio-sclerosis is caused by slowing of the blood 
current produced by changes of the circulation in the capillary 
vessels. 

It appears to me that the most practical way to look at all these 
morbid changes in the arteries is to consider them the results of a 
combination of chronic productive inflammation and of degeneration 
occurring in connective. tissue. We shall then think of the arteries 
as we do of the heart or the liver or the kidneys, as a definite part 
of the body, liable to become the seat of chronic inflammation from 
the same causes as those which produce similar changes in other 
parts of the body. 



"'•%m^^^. 




y 






Fig. 215.— Chronic Arteritis. 
Inner coat thickened— cerebral artery. 

In all the arteries the wall is composed of an outer connective-tis- 
sue coat supplied with blood vessels, of a middle coat formed of 
smooth muscle, and of an inner connective-tissue coat not suppHed 
with blood vessels. In the small arteries inflammation simply causes 
the formation of new tissue ; in the large arteries and in the aorta, 
besides the formation of new tissue, there is also the death and de- 
generation of tissue. 

There is sufficient difference between the chanires in tlu- small 
arteries, the large arteries, and the aorta to make it convenient to 
described them separately. 

1.^ The Small Arteries.— (a) The simplest change in the small 
arteries is an increase in the size and number of the endothelial cells. 



41(3 



THE VASCULAR SYSTEM. 



This is best seen in the arteries in iniharY tubercles and in small 
gummata. 

(6) There is a growth of new connective tissue from the endothe- 
lium which encroaches upon the lumen of the artery and finally oc- 
cludes it. The growth is composed of large branching cells, small 
round cells, and basement substance ; later the cells become smaller 
and less numerous, the basement substance denser. The growth 
forms a ring on the inside of the intima which is not symmetrical, but 
is thicker in some one place. This change always narrows the calibre 
of the artery, and, when far advanced, occludes it. It is seen very 
frequently in the small arteries in every part of the body. It is often 
called ^'obliterating endarteritis'' (Figs. 215 and 216). 




Fig. 216.— Chronic Obliterating Ent) arteritis. 
The lesion in this case is excessive, almost entirely closing the lumen of the vessel. There is, 
too, a moderate degree of periarteritis. 

(c) There is a thickening of the inner coat beneath the endothe- 
lium. The change begins by a growth of cells and a splitting-up of 
the basement substance in the intima immediately beneath the endo- 
thelium. Then there is a growth of basement substance, with but a 
moderate number of cells, which renders the inner coat thicker and 
thicker until the lumen of the artery is considerably narrowed, but 
yet the arterv is not occluded. The endothehal cells may remain in 
place and unchanged over the thickened intima. This change is of 
very frequent occurrence, so that it is easy to see all the stages of the 
growth, from the first splitting-up of the intima until it is changed 
into a dense thickening. 

(d) The thickening of the inner coat just described, instead of 
occurring, by itself, may have joined with it either a thickening of 



THE VASCULAR SYSTEM. 



417 



the muscular coat alone or a thickening of both the muscular and 
outer coats. 

(e) There is a thickening of the intima, a replacement of the mus- 
cular coat by connective tissue, and a thickening of the outer coat. 
This can properly be called a ^^ sclerosis " of the artery. 

2. The Large Arteries. — In the large arteries altogether the 
most frequent change is the thickening of the intima. This is often 
present in arteries which look normal to the naked eye. But besides 
the thickening of the intima there is often in addition a thickening 
of the middle and outer coats, or a renlacement of the muscular coat 












.-'' 



Fig. 217.— Chronic Arteritis. 
Inner and middle coat thickened— radial artery. 



hy connective tissue. When all the coats are thickened in this way 
the arteries often become elongated and tortuous. Occasionally 
there are areas of degeneration in the thickened wall of the artery, 
or even infiltration with the salts of hme. 

The Aorta.-— T\\Q changes in the aorta differ from those in the 
arteries b}^ reason of the combination of degeneration and necrosis 
with the growth of new tissue due to the chronic inliammation. by 
the frequency of calcification, and by the liability of the outer coat to 
purulent infiltration. We find, therefore, in the aorta . 

{a) Simple thickening of the inner coat by uoav ccHuux'tive tissue. 

{h) Degeneration and softening of the inner and middle coats. 



418 



THE VASCULAR SYSTEM. 




Fig. 218. — Cheo>t:c Ikflamhatiox of the Aorta. 
Inner coat thickened an'd necrotic; middle coat calcified and necrotic. 




b-l 



Fig. 219, — ^Atheroha of the Aorta, \rtTH DEGE>rEiRATiox of New-formed Tissue. 
a. adrentitia: 6, media: c, new tissue derelopted in the intima; d, degenerated area: e. area of 
softening; g, fat droplets in softened area. 



THE VASCULAR SYSTEM. 



419; 



(c) Calcification of the inner and middle coats. 

(d) Infiltration of the outer and middle coats with pus cells. 

(e) Thinning and atrophy of the inner and middle coats. 

(/) The formation of thrombi on the roughened surface of the 
inner coat. 

Inflammatory changes in the aorta associated mth degeneration, 
calcification, etc., are often called ^* atheroma^'' (see Figs. 218 and 
219). 




Fig. 220.— Tubercular Arteritis in the Lung. 
Showing the encroachment of an area of tubercular inflammation upon the wall of the arterjr 
and the formation of a mass partly occluding the lumen of the vessel. This section shows how 
the generalization of the tubercular inflammation through Uie body may occur by the sweeping 
away of the tubercle bacilli by the blood and the establishment of new foci in various parts of the 
body. From specimen prepared by Dr. J. S. Ely. 

Tubercular LiflcDnniatioii of the Arteries. 

In tubercular inflammation the walls of tlie arteries, particularly 
the smaller ones, may be thickened and their lumiiia obliterated 
(Fig. 220). 

DILATATION AND ANEURISM. 

1. Cirsoid aneurism, consists in the dilatation and lengthening 
of largo or small arteries. The walls of the artery are thinned, the 
vessel is tortuous and in places sacculated. These changes are most 
frequent in small arteries, especially the temporal and occipital. 



420 THE VASCULAR SYSTEM. 

'They involve tlie trunk of the vessel and its branches, or may extend 
to the capillaries and small veins. They form larger or smaller 
tumors beneath the skin. 

Karely they are found in the larger arteries, and even in the 
aorta. 

2. The ordinary aneurism is a dilatation of the coats of the artery 
>over a larger or smaller part of its course. Such dilatations are usu- 
' ally due to chronic endarteritis and atheroma. According to their 
shape we may distinguish two varieties : the diffuse and the circum- 
scribed. 

(a) The diffuse, cylindrical, or fusiform aneurism consists in a 
uniform dilatation of all the coats of an artery, so that it assumes the 
shape of a fusiform or cylindrical swelling. In the walls of the 
dilated portion of the vessel there are often smaller, circumscribed 
dilatations. The wall of the aneurism is atheromatous or calcified ; 
the middle coat may be atrophied. The arch of the aorta is the most 
common seat of this form of aneurism, but the entire length of the 
aorta, or parts of any other arteries, may be dilated in the same way. 

(b) The circumscribed or sacculated aneurism consists either in a 
dilatation of the entire circumference of an artery over a short por- 
tion of its length, or in a dilatation of only a small portion of one 
side of the wall, so that the aneurism looks like a swelling attached 
to one side of the artery. The aneurism commences as a dilatation 
•of all the coats of the vessel ; but as soon as it attains any consider- 
. able size the middle coat atrophies, so that the wall is composed of 
the inner and outer coats ; or the inner coat is destroyed by endar- 
teritis, so that the outer coat alone forms the wall of the aneurism. 
As the aneurism increases in size it presses upon and causes the de- 
.struction of the neighboring tissues and viscera, and portions of these 
tissues and viscera become incorporated with, or take the place of, the 
wall of the aneurism. The cavity of the aneurism is filled with fluid 
or clotted blood, or with layers of fibrin which adhere closely to its 
wall. The communication between the aneurism and the artery may 
be small or large. If arterial branches are given off from the aneu- 
rism they may remain open or become plugged with fibrin ; or their 
walls are thickened and their cavities narrowed by endarteritis. 
Death is produced by the pressure and interference of the aneurism 
with the adjoining ■\ascera, or by rupture. The rupture may allow 
enough blood to escape to destroy life, or the blood may be held in by 
the soft parts and a second false aneurism formed about the original 
vone. 

Dissecting aneurisms are those in which, owing to a solution of 
-continuity of the inner layers of the artery, the blood gets between 
•the media and adventitia, and forces its way for a greater or less 



THE VASCULAR SYSTEM. ^ 421 

distance between them. Or it may separate the media into two 
layers. 

ANEURISMS OF THE DIFFERENT ARTERIES. 

The aorta may be dilated over its entire length, or there may be 
diffuse or circumscribed dilatations at any portion of its course ; or 
there may be several aneurisms, situated at different points. The 
ascending portion of the arch of the aorta may be uniformly dilated 
in a fusiform shape, or there may be circumscribed dilatations on its 
anterior wall, or, more rarely, on its posterior wall. The sacculated 
aneurisms may be of all sizes and may rupture within the pericar- 
dium ; or they may form a cavit}^ in the upper part of the ventricular 
septum and communicate by openings into the pulmonary artery and 
left ventricle ; or they may dilate downward between the visceral 
and parietal pericardium, in front of the heart, pushing that organ 
backward. They may perforate into the right or left auricle or right 
ventricle, the superior vena cava, or the pulmonary artery ; or they 
may reach a large size, press on and erode the right side of the 
sternum and adjoining ribs, project under the skin, and even rup- 
ture externally. 

The transverse portion of the arch may be dilated in a fusiform 
shape, or there may be sacculated aneurisms at any point in its wall. 
The sacculated aneurisms usually reach a considerable size. They 
press on the sternum and ribs in front, or on the oesophagus, trachea, 
and bronchi behind. The large arteries given off from the arch lYio^y 
be occluded. They cause death by pressure on the air passages, the 
oesophagus, and the vena cava ; or may rupture externally or into 
the oesophagus, trachea, bronchi, or pleural cavities. 

On the abdominal aorta we usually find aneurisms sacculated^ 
If they are situated high up they may project into the pleural ca^d- 
ties ; if lower down, into the abdomen. They may compress and dis- 
place the viscera, vessels, and nerves, and erode the vertebrjie. They 
may rupture behind the peritoneum, into the peritoneal cavity, the 
pleural cavities, the inferior vena cava, the lungs, the colon, the 
pelves of the kidney, or the posterior mediastinum. 

The coronary arteries may be dilated throughout, or may be the 
seat of small sacculated aneurisms. These may rupture into the 
pericardium, or may cause rupture of the heart wall. 

The pulmonary art ernes are rarely the seat of aneurisms. Dif- 
fuse and circumscribed dilatations, however, sometimes occur on the 
main trunk and on the two principal branches of the artery. They 
do not usually reach a large size, but may cause death by rupture. 
General dilatation of all the branches of the pulmonary artery is 
more common. It is found in connection with stenosis of the mitral 
valves and with compression or induration of the lung tissue. 



422 ^ THE VASCULAR SYSTEM. 

Of the other arteries of the body there is hardly any one which 
may not become the seat of an aneurism, but those of the pophteal 
artery are most common. - 

STENOSIS. 

Stenosis and obhteration of the aorta, at the point of entrance of 
the ductus arteriosus, have been described in a considerable number 
of cases. 

The situation of the stenosis is either exactly at the entrance of 
the ductus arteriosus or close on either side of this point. The de- 
gree of stenosis varies. The aorta may be entirely closed and con- 
verted into a solid cord for a length of half an inch ; or there may 
be a circular constriction through which there is a larger or smaller 
opening — the constriction is uniformly circular ; or there is a septum 
springing from the concave side of the vessel at the opening of the 
ductus arteriosus ; or there is a cicatricial -like contraction of the aorta. 
The walls of the aorta at this point may be thickened and sclerosed. 
The ductus arteriosus may be closed or open. Above the constriction 
the aorta is usually dilated ; below it, it is normal, dilated, or ste- 
nosed. 

Stenosis of the aorta produces hypertrophy of the left ventricle, 
and, later, of the right ventricle, with venous congestion through- 
out the body ; or there may be a collateral circulation developed be- 
tween the arteries given off above and below the constriction ; or 
there may be rupture of the aorta, the right ventricle or auricle. 

This condition is found at all ages, but is produced during foetal 
'life or in the first year of extra-uterine life. It is probable that it 
may be caused after birth by an abnormal closure of the ductus ar- 
teriosus. This vessel normally becomes closed without the forma- 
tion of a thrombus. If a thrombus is formed it may extend into the 
aorta and obstruct it ; or the ductus arteriosus is filled with a throm- 
bus, but increases for a time in size ; afterward, as the thrombus is ab- 
sorbed, the vessel contracts and draws the walls of the aorta together. 

Stenosis of the aorta and of some of the other arteries has been 
observed, in a few rare cases, without any known cause. 

Endarteritis, with the production of atheromatous and calcareous 
patches, may obstruct or entirely obliterate the smaller arteries. 
This is especially seen in the arteries of the leg, foot, and brain, and 
in the coronary arteries. The writer has seen a case in which the 
subclavian was completely occluded in this way. 

Narrowing of the aorta and of all its branches, with thinning of 
the arterial coats, is found as a congenital condition. It usually oc- 
curs in females, in connection with imperfect development of the 
whole body. 

Stenosis from thrombosis or embolism is treated of elsewhere. 



THE VASCULAR SYSTEM. 423 

RUPTURES AND WOUNDS. 

Rupture of arteries may occur under the following conditions : 

1. Fatty degeneration or endarteritis, with atheromatous changes, 
may so soften and destroy the inner and middle coats of an artery 
as to admit of its rupture. The aorta, just above the valves, is the 
most frequent seat of this lesion. The rupture may run in any di- 
rection its edges are irregular and jagged. The blood may burst 
through all the coats of the aorta at the same point ; or, more fre- 
quently the external coat remains and the blood is infiltrated in the 
middle coat and between it and the external coat. In this way a 
dissecting aneurism is formed, which may extend along the aorta 
for a considerable distance. After a short time the external coat 
usually gives way at some point, and the blood escapes. In rare 
cases life is prolonged for some time, the rupture being closed by a 
new membrane. 

We also find ruptures from fatty degeneration and atheroma in 
the arteries of the brain and lungs ; in the coronary arteries, the 
coeliac axis, the mesenteric arteries, and in the arteries of the ex- 
tremities 

2. In rare cases stenosis of a portion of the aorta may cause 
rupture at some point between the seat of stenosis and the heart. 

3 Contusions, wrenchings, and severe falls may rupture the 
walls of an artery, either partially or completely, producing trau- 
matic or dissecting aneurisms, or completely severing the vessel. 

4. Penetrating wounds may injure or entirely sever an artery. 
If the vessel be large and the injury severe, death from haemorrhage 
is the usual result. A small artery may become closed or be the seat 
of a false aneurism. 

In the healing of a wounded artery two conditions co-operate. 
The vessel retracts and contracts, and a thrombus is formed within 
it. The contraction may be alone sufficient to close the vessel ; its 
coats thicken, and the inner surfaces finall}" are fused together ; or 
the blood coagulates and forms a thrombus in the vessel near the 
wound. This thrombus later becomes organized and the vessel is 
converted into a fibrous cord. 

Spurious or false aneurisms are found most frequently con- 
nected with vessels of the extremities. When an artery is wounded 
the blood escapes into the surrounding soft parts, and a cavity is 
formed filled with blood and broken-down tissue. This condition 
may terminate in several ways. 

(rt) The wound in the artery may heal and the effused blood be 
absorbed. 

{})) The effused blood and broken tissues may become gangrenous 
and the surrounding soft parts be inflamed. 



424 THE VASCULAR SYSTEM. 

(c) A sort of sac wall may be formed by the soft parts, while the 
wound of the artery remains open, so that we have an aneurismal 
sac through which the blood is constantly pouring. 

5 If an artery be wounded, and at the same time the vein which 
accompanies it, we have as the result the conditions called aneu- 
rismal varix and varicose aneurism. In aneurismal varix the artery 
and vein become adherent at the seat of injury, so that the arterial 
blood passes directly into the vein. There is a smooth, rounded 
opening between the two vessels, the vein is dilated into a sac, and 
the veins emptying into it are dilated and tortuous. 

In varicose aneurism the artery and vein do not communicate di- 
rectly, but a false aneurismal sac is formed between the vessels, into 
which the blood is poured before passing into the vein. 

Varicose aneurism may also be produced by the spontaneous rup- 
ture of an aneurism into a vein. The aneurism presses against the 
vein, becomes adherent, and finally ruptures into it. This condition 
has been observed between the aorta and pulmonary artery ; the aorta 
and inferior and superior vena cava ; the popliteal artery and vein ; the 
femoral artery and vein ; the splenic artery and vena azygos ; the in- 
ternal carotid and sinus cavernosus. Even in cases of perforation 
by aortic aneurisms life is usually prolonged for some time. 

6. Destructive inflammation or tumors of the surrounding tissues 
may invade and destroy a portion of the wall of an artery. Thus 
ulceration of the trachea, bronchi, bronchial glands, and oesophagus, 
or tumors of these parts, may perforate the aorta ; gangrene of the 
lungs, the pulmonary arteries; ulcer of the stomach, the gastric 
arteries, etc. 

TUMORS. 

Secondary tumors, chiefly carcinomata and sarcomata, may occur 
in the walls of the arteries by continuous growth from without, 
involving first the external layers. To these layers they are usually 
confined, for the density of the inner layers affords such marked 
resistance to the infiltration of the tumor cells that they are apt to 
pass intact through the tumor, which grows around them. More 
frequently the arteries become secondarily involved in the growth 
of malignant tumors by the occurrence within them of emboli 
formed by larger and smaller masses of tumor cells. 

These emboli are usually of small size, and are apt to get into the 
circulation by growing through the walls of the veins into their lu- 
mina. Large emboli from tumors are most apt to occur in the branches 
of the pulmonary artery. The emboli, formed as they are for the 
most part by cells capable of growth and proliferation, are apt to soon 
form connection with the walls of the vessels, and, by the growth 



THE VASCULAR SYSTEM. 42o 

into them of blood vessels from the vasa vasorum to find the condi- 
tions necessary for their development, and they may thus soon in- 
volve the entire wall of the vessel and grow out into adjacent parts. 



THE VEINS. 

• DILATATION. 

Dilatation of the veins, or phlebectasia, presents itself under a va- 
riety of forms. 

1. Simple Dilatation. — The vein is uniformly dilated in a cylin- 
drical or fusiform shape ; its length is not increased ; its walls are of 
no:?mal thickness or thinned ; the valves increase in size, or are in- 
sufficient, or atrophic, or are torn. 

2. Cirsoid Dilatation. — The vein is uniformly cylindrically di- 
lated, but is also increased in length, so that it assumes a very tor- 
tuous course. The walls are normal, thickened, or thinned. 

3. Varicose Dilatation. — A circumscribed portion of the wall of 
the vein is dilated so as to form a globular sac. The sac communi- 
cates with the vein through a large or small opening. The wall of 
the sac is formed of the coats of the vein, which preserve their nor- 
mal thickness, are thickened or thinned ; the middle coat may dis- 
appear entirely. There may be only one such dilatation, or there 
may be a number on the same vein, or a number of veins may be af- 
fected at the same time. The vein may be otherwise normal, or, 
more frequently, is dilated in the cirsoid form. 

4. Anastomosing Dilatation. — A number of contiguous and 
anastomosing veins are dilated, both in the cirsoid and varicose 
forms. The vein then looks like a series of cavities separated by 
thin partitions. The dilatations of the same vein become adherent 
to each other and to those of the adjoining veins ; portions of the 
wall of the dilated parts may disappear, and we find a number of 
cavities containing venous blood and separated from each other by 
thin partitions. The course of the vein can no longer be followed 
out. 

Spontaneous cure of dilatations of the veins is not common, and 
usually occurs only in the lesser degrees of the lesion. Most phle- 
bectasic© increase steadily in size and extent. Very frequently 
thrombi form in the dilated veins, and either partially or completely 
fill them ; and these in rare cases mav become ori;"anized, or the 
clots may dry and become calcified, forming pJileholifJis (see page 
()()), and, by the formation of ncAV connectiA^e tissue in the walls, 
they may become enclosed in a fibrous capsule, with the oblitera- 
tion of the vessel. The wall of the dilated sac may become so thin 
3S 



4'2G THE VASCULAR SYSTEM. 

that it finally ruptures, and the blood is discharged externally. 
Sometimes inflammation is set up in the tissues surrounding the 
vein, and ^ye find both the surrounding tissues and the wall of the 
vein the seat of purulent infiltration or fibrous thickening, Tho 
parts of the body from which the dilated veins draw their blood may 
exhibit the results of chronic venous congestion, oedema, hypersemia, 
and hypertrophy or ulceration. 

When occurring in mucous membrane, dilated veins are usually 
associated with persistent catarrh. There is hardly one of all the 
veins of the body which may not be dilated. The hfemorrhoidal 
veins ; the veins of the leg and thigh ; those of the pelvis and pelvic 
viscera ; those of the spermatic cord, scrotum, and labia ; those of 
the abdominal wall ; those of the neck and arms — are the ones most 
frequently found in this condition. 

The causes of dilatation are principally some mechanical obstruc- 
tion to the passage of the blood through the veins toAvard the heart ; 
but changes in the walls of the vessels from inflammation or injury, 
etc. , are not Avithout influence. 

WOUXDS— RUPTURE. 

Wounds of the veins usually heal by a simple contraction and 
an adhesive inflammation of their walls ; sometimes by the forma- 
tion of a thrombus. Rupture of the veins may be produced by se- 
vere contusions and crushings of the body and by \dolent falls. 
Perforation of a vein may be produced by suppuration of the soft 
parts and the invasion of the walls of the vessel ; by the pressure of 
an aneurism or of a new growth ; by the thinning of the wall of 
the vein ii> phlebectasia. 

INFLAMMATION. 

Inflammation of the veins, phlebitis, may involve chiefly the ex- 
ternal layers — periphlebitis ; or the internal — endojohlebitis ; or, 
as is very frequently the case, the entire wall may be affected. 
Phlebitis may be caused by the presence of a thrombus, by injuries, 
or by an inflammation of t-lie surrounding tissues. Thrombosis of 
the vein, either primary or secondary, is a very constant accompa- 
niment of phlebitis. 

Acute Phlebitis may commence as a suppurative periphlebitis or 
as a result of inflammatory processes about the vessel. The outer 
layers of the venous wall are congested, swollen, inflltrated with se- 
rum and pus. The inner coats may become infiltrated with pus ; 
they may become necrotic and disintegrate. A thrombus is con- 
stantly formed under these conditions, which may for a time stop 



THE VAHCULAK SYSTEM. 



427 



the circulation and keep the products of inflammation and degenera- 
tion from mixing with the blood ; but the thrombus itself is prone to 
disintegration, and thus the exudations and decomposing fragments 
of tissue may enter the circulation. 

On the other hand, owing to the presence of irritating or infec- 
tious material within the vein and the formation of a thrombus, the 
inflammatory process may be at the commencement an endophlebi- 
tis, bat usually, if the inflammation be at all severe, the entire wall 
of the vessel will eventually be involved. The pus cells in both 
cases doubtless come from emigration from the vasa vasorum. 
Acute phlebitis may terminate in the absorption of the thrombus and 
the return of the vein to its normal condition ; in the obliteration of 
the vein ; or portions of the thrombus may become detached and find 
their way as emboli into various parts of the body. The most im- 




FiG. 221.— Tubercular Phlebitis. 

The section is from one of the pulmonary veins in a child dead of acute general miliary tuber- 
culosis. Specimen loaned by Dr. W. P. Northrup. 



portant results of phlebitis are usually those which depend iipon the 
introduction into the blood of these emboli or of septic material (see 
Thrombosis and Embolism, page 59, and Pytemia). 

Chronic periphlebitis produces thickening, principally of the outer 
coats of the veins, but the inner coats may also be involved. The 
surrounding tissue may be also thickened and coalesce with the 
walls of the vein. There may or may not be thrombosis. 

Chronic endophlebitis is a not very common lesion, of the same 
general character as chronic endarteritis. More or less circum- 
scribed patches of new connective tissue are formed in the inner 
coats, which may undergo fatty or calcareous degeneration. 

Tuherciilar Iiiflanunafion of the walls of the veins may occur 
as an extension of the process from without or from a lodgment of 
the tubercle bacilli in the blood current on the intima (Fig. -^21). 



438 THE VASCULAR SYSTEM. 

This is not infrequent in the pulmonary veins, and Weigert has called 
attention to the fact that in acute miliary tuberculosis the growth 
of tubercle tissue into the lumina of these veins from tubercular 
lymph nodes is of frequent occurrence and readily explains the 
topography- and mode of occurrence of the general disease. The tu- 
bercle bacilli which are present in the tubercular tissue growing 
into the lumen of the veins find thus an easy distribution. 

Sypliilitic Inflammation may involve the walls of the veins 
either as gummy tumors or as more diffuse thickenings. 

TUMORS. 

Primary tumors of the veins are rare. Small leiomyomata have 
been described in the saphenous and ulnar veins. A myosarcoma 
as large as a man's fist has been described, situated in the dilated 
vena cava inferior. The veins are not infrequently secondarily in- 
volved by sarcomata and carcinomata, and sometimes by ckondro- 
mata. The thin walls of the veins offer comparatively little resist- 
ance to the encroachment of malignant tumors, which thus gain 
access to the circulation and may form metastases in various parts 
of the body. 

PARASITES. 

JEchinococcus is sometimes found in the veins, having either de- 
veloped there or pe'rforated from without. 

Two species of distoma {liver fluke) occur in man. D. Jiepati- 
cum occurs rarely in man, and, while usually found in the bile ducts, 
may occur in the vena cava. D. Jicematobium is very common in 
man in Egypt and in other parts of Africa, and usually occurs in the 
portal vein or its branches, and frequently in other veins. 

THE CAPILLARIES. 

The walls of the capillaries are so thin and so intimately con- 
nected with the surrounding tissues that their lesions are studied 
most appropriately among the diseases of the several organs. Dila- 
tation of the new-formed capillaries in tumors, granulation tissue, 
etc., and fatty and hyalin degeneration of their walls, may be 
mentioned here as readily observed lesions occurring under a variety 
of conditions. The changes which we assume to occur in the walls 
of the smaller veins and capillaries in exudative inflammation, by 
reason of which fluids and blood cells pass through them, are not yet 
sufficiently understood to be described with definiteness. 

THE LYMPH VESSELS. 
The smaller lymph vessels can hardly be treated as independent 



THE VASCULAR SYSTEM. 420 

structures, since their walls are so closely joined with the tissues 
through which they pass ; the lymph radicles, indeed, being nothing 
more than the spaces in the connective tissue in which the variously 
shaped connective-tissue cells lie. In the larger lymph vessels we 
find a moderate number of more or less independent lesions. 

- INFLAMMATION. 

Lymphangitis. 

Inflammation of the larger lymph vessels is usually secondary 
and connected with some wound or injury. Owing, it is believed, 
to the entrance into the lymph trunk of some septic material or bac- 
teria, the vessels, sometimes for a considerable distance away from 
the wound, become red, tender, and painful. Under these condi- 
tions the microscopical appearances which the vessels present vary. 
In some cases the redness disappears after dearth and we find no ap- 
preciable alteration. In other cases we find the walls of the lymph 
vessels more or less densely infiltrated with pus cells, and the lumen 
may contain variable quantities of pus and fibrin and desquamated 
endothelium. The tissue about the vessels may also be infiltrated 
with serum and pus. These lesions may undergo resolution and the 
vessel be restored to its normal condition ; or the vessel wall and sur- 
rounding tissue may die or become involved in abscess ; or new con- 
nective tissue may form in and about the vessel, sometimes with 
obliteration of its lumen. The lymph nodes may participate in the 
inflammatory process. 

Inflammation of the lymph vessels may occur as the result of dis- 
section and other wounds, and the bites of venomous reptiles. It 
may occur in the uterine lymphatics in the phlegmonous form of puer- 
peral fever, and under other conditions. 

Tubercular Lijnipliangitis. — Tubercular inflammation occurs 
both in large and small lymph vessels. Miliary tubercles and dilf use 
tubercle tissue may form in the walls and project into the lumen of 
the larger trunks ; or in the smaller vessels the new growth may en- 
tirely fill the lumen, and grow in this, with more or less involvement 
of the walls. This may occur independently, but it is most fre- 
quently seen in connection with tubercular inflammation of adjacent 
tissues. Thus from tubercular lymph nodes in the vicinity of the 
thoracic duct there may be a direct extension of the tubercular in- 
flammation, ail involvement of the walls of the duct, and a growth 
of tubercle tissue into its lumen. Such growths in the thoracic duct 
have been shown by Weigert to be frecjuent in acute general miliary 
tuberculosis, and verv satisfactorilv explain the dissemination of the 
tubercle bacilli. Li the vicinitv of tubercular ulcers in the intestines. 



430 THE VASCULAR SYSTEM. 

furthermore, vre often see the subserous lymph vessels, which pass 
from the vicinity of the ulcers, distended with the products of tuber- 
cular inflammation and looking like dense white knobbed cords. 

Syphilitic Inflammation oi the lymph vessels not infrequently 
occurs in the ^-icinity of syphihtic ulcers in the primary stage. In 
later stages there may be thickening of the walls of the vessels and 
the development of gummy tumors in and about them. 

LYMPHAXGIECTASIS. 

Dilatation of the lymph vessels occurs under a variety of condi- 
tions. It may be congenital, or it may be due to some hindrance to 
the flow of lymph onward — as by pressure from any cause, or from the 
occlusion of the vessels by inflammation — or it may be produced by 
imknown causes. If the dilated vessels form a circumscribed mass, 
this is often called a lymphangioma (Fig. I'^T). In certain forms of 
elephantiasis and in macroglossia the dilatation of the h-raph ves- 
sels is an important factor. Its occurrence is not infrequent in the 
labia. 2^1'epuce, and scrotmn. 

TUMORS. 

The relation of the endothelium of the lymph vessels and spaces 
to endotheliomata has been already mentioned in the section on 
Tumors. 

The dissemination of malignant tumors through the lymi^li chan- 
nels is of frequent occurrence, and is particularly marked in the case 
of carcinoma. In the "\4cinity of carcinomata the lymph vessels are 
not infrequently crowded with the tumor cells, forming white, irreg- 
ular cords ; or small masses of the tumor cells may be found in the 
lymph vessels, either near to or remote from the tumor. White, 
irregular networks are often formed in this way beneath the pleura 
in carcinoma of the lung (Fig. 131). or beneath the capsule of the 
liver. Transverse sections of lymph vessels thus distended show 
sometimes swelling and detachment of the endothelium and a crowd- 
ing of the lumen with tumor cells. AVhether or not the endothelium 
participates in the new formation of the characteristic carcinomatous 
cells is not known. 

THE LYMPH XODES {Lymph Glands).' 

It is well, in stud^'ing the lesions of the lymph nodes, to remember 
that they are structures so placed in the course of the lymph vessels 

^ "What we call lymphatic tissue embraces not only the so-called lymph glands and 
the less complex but still well-defined structures found in the stomach, intestines, 
tonsils, and elsewhere, and called lymph follicles, but also the less well-defined, 



THE VASCULAR SYSTEM. 431 

that the lymph, in flowing toward the larger central trunks, passes 
through them, undergoing a sort of filtration as it percolates through 
the trabeculsB of the lymph sinuses. If this simple fact be borne in 
mind the diseases of the lymph nodes, which are in the majority of 
cases secondary, are much more readily understood. Particles of 
pigment which in any way get into the lymph vessels are carried 
along until a lymph node is reached, and here they are, in part at 
least, deposited among the trabeculse of the sinuses, while the lymph 
passes on and out of the efferent vessels (Fig. 223). The same thing 
occurs when cells from malignant tumors, bacteria of various kinds, 
etc., gain access to the lymph vessels; and also, as there is good 
reason for believing, in tha case of many poisonous materials which 
our present knowledge does not enable us to associate with bacteria. 
These various materials, filtered out of the lymph by the glands, may 
act in a variety of ways to produce lesions in them. 

INFLAMMATION. 

Acute Inflammation of the lymph nodes usually occurs in con- 
nection with some inflammatory process in the region from which its 
lymph is gathered. The nodes are in the majority of cases swollen, 
reddened, and softer than normal, and often the seat of smaller and 
larger hgemorrhages. Sometimes one, sometimes several nodes of a 
cluster are affected. 

The microscopical examination shows the most prominent change 
to be a great increase in the number of cells in the follicles and cords. 
as well as in the lymph sinuses. These cells are, in part, small and 
spheroidal, and similar to those normally filling the meshes of the 
follicles ; in part large polyhedral or variously shaped cells with 
prominent nuclei ; the latter cells are most abundant in the lymph 
sinuses (Fig. 222), In addition to this there is swelling of the endo- 
thelial cells of the reticulum of the sinuses. The blood vessels may 
be distended with blood, or there may be blood, in greater or less 
quantity, free in the sinuses and follicles. The origin of the large 

irregular masses of tissue resembling that of lymph follicles, which, as Arfiold has 
shown (Virchow's Archiv, Bd. Ixxx., p. 315; Bd. Ixxxii., p. 394; Bd. Ixxxiii., p. OSO; 
Bd. Ixxxvii., p. 114), is widely disseminated in variable amounts in different parts of 
the body; iuthehmgs; beneath the pleura, and elsewhere ; in the liver, kidneys, ete. 
Although the exact nature of these more diffuse masses of lymphatic tissue is too 
little understood, as indeed is that of the lymph follicles and glands themselves, there 
is reason to believe that they are, analogous structures and prone to be affected In- 
similar deleterious agencies. It seems better, in view of the fact that the so-called 
lymph glands are not glands at all, in the ordinary sense of the word, to call them 
lymph nodes, amX the smaller masses of lymphatic tissue scattered through various 
parts of the body lymph iwduks instead of " iymph follicles." 



432 



THE VASCULAR SYSTEM. 



number of new cells which may form in a very short time is not yet 
definitely known. They may be emigrated leucocytes or their de- 
rivatives ; they may be derivatives of the endothelium of the reti- 
culum ; or they may be in some cases, at least in part, cells which 
have been brought into the node, through the afferent trunks, from 
some external inflammatory focus. The capsule of the nodes, and 
not infrequently the connective tissue about them, may also be in- 
filtrated with round cells. 

Acute inflammation may terminate in resolution, the new cells 
disappearing either by fatty or other degeneration, or by being car- 
ried off in the lymph, and the node return to its normal condition. 




222.— Acute Inflammation of Lymph Node in Typhoid Fever. 
Showing a portion of one of the mesenteric nodes. A, capsule; B, perifollicular space or 
iymph sinus, containing in its meshes many large cells; C, portion of one of the follicles, with large 
and small cells in the meshes of its reticulum. 

This is the rule in the less intense forms of inflammation. On the 
other hand, the inflammatory process may become purulent and so 
intense as to lead to the formation of abscess, usually with a greater 
or less involvement of the tissue about the nodes. There may be at 
first numerous small abscesses, which coalesce to form larger ones. 
These abscesses — buboes — may open externally or internally, or they 
may become dried and converted into cheesy masses which may cal- 
cify and, by a chronic inflammation in their periphery, become en- 
closed by dense connective tissue. Sometimes, instead of abscess 
being formed, the tissue of the inflamed nodes becomes necrotic and 



THE VASCULAR SYSTEM. 



i 0'> 



breaks down, inducing more or less severe inflammatory or necrotic 
changes in the tissues in their vicinity. 

In still other cases acute inflammation of the lymph nodes 
jjasses into the chronic form. 

Moderate degrees of inflammation in the lymph nodes are very 
common in connection with various forms of inflammation in neigh- 
boring parts. Thus simple pharyngitis, gastro-enteritis, erysipelas, 
simple purulent inflammation, etc., are often associated with this 
lesion of the nodes. The lymph nodes of children are, as a rule, more 
easily affected by moderate inflammations in neighboring parts than 
are those of adults. Purulent inflammation of the lymph nodes is 
most frequently associated with severer forms of inflammation of 
adjacent or related parts, especially those of an infectious character, 




^-fi^S^^. \ - ■> ■■■'■/'' ;'v:' v!^'«-ssTi@s^iA';>: -■ ■ ■ -■•■'■ 



m^. 








i^-i^if=toH^&^^^^^ 



:SSWl'^ 



■ I , ■>.•:'",<', ^. ■•<'.. ■^[■~ :-■: -- •-. 



Fig. 223.— Chronic Inflammation of Bronchial Lymph Node. 

Showing obliteration of the lymph sinuses and atrophy of the lymph follicles by the new-formed 
connective tissue. 

s^'philitic inflammation, poisoned wounds, pyaemia, etc. In a cer- 
tain number of cases we find bacteria in the inflamed lymph nodes, 
either singly or in zoogloea colonies, which have presumably some- 
thing to do with the lesion. 

In many cases the lesion of the lymph nodes appears to be in- 
duced, not by bacteria in the nodes themselves, but by poisons pro- 
duced elsewhere by the action of bacteria and brought to the nodes 
by the Ij^mph. The swelling of the lymph nodes in typlund fever 
and diphtheria is probably induced in this way. N"ecrotic areas in 
the Ij'inph nodes may result from the presence of bacterial poison. 

Chronic JnHamiiud ion.— This is characterized bv the increase of 



434 



THE VASCULAR SYSTEM. 



the connective-tissue elements of the node, with a gradual and com- 
mensurate disappearance of the lymphoid cells. The reticulum of 
the follicles and sinuses becomes thickened and fibrous, and in the 
trabeculse and capsule new connective tissue is formed, until, in ad- 
vanced cases, the entire node may be more or less completely con- 
verted into a mass of connective tissue. This condition is very fre- 
quently seen in the lower tracheal and in the bronchial nodes, 
apparently as a result of the lodgment in them of respired pigment 
particles ; but it may occur in any nodes, either as a result of re- 
peated moderate degrees of inflammation or from causes which we 
do not know. In some cases the nodes are greatly enlarged and the 
new tissue contains many large cells, while in other cases the con- 
nective tissue is dense and contains but few cells (Fig. 223).' 










Fig. 2;;4.— Pigmentation of Bronchial Lymph Node. 
The pigment is largely in the lymph sinuses and enclosed in cells. A, capsule of node; B, 
lymph follicle; C, perifollicular lymph sinuses. 



Pigmentation. — The pigment which is very frequently found in 
lymph nodes may be derived from the hsemoglobin of the blood, 
either in the nodes themselves or in remote parts, or it may be 
formed of various materials introduced into the body from without, 
such as the pigments used in tattooing, respired dust particles of va- 
rious kinds — coal, stone, iron, etc. (Fig. 224). The pigment particles, 
which usually first lodge in the lymph sinuses, may collect here in 
large quantities, either in the reticulum or the cells lying in its 



^ Consult liibbert, " Ueber Regeneration und Entziindung der Lymphdriisen, " 
Ziegler's Beitrage zur path. Anat., Bd. vi., 1889, p. 187. 



THE VASCULAR SYSTEM. 435 

meshes , they may penetrate the folKcles and cords and find perma- 
nent lodgment there. They usually induce a greater or less degree 
of chronic inflammation, so that in extreme cases, such as are fre- 
quently seen in the bronchial lymph nodes, nothing is finally left of 
the node but a more or less deeply pigmented mass of dense connec- 
tive tissue. The function of the node is, of course, in this way par- 
tially or entirely destroyed. The pigment in these cases appears to 
reach the node, in part by being carried along free in the lymph cur- 
rent, in part by becoming enclosed in leucocytes and being trans- 
jDorted by them. Pigmentation of the nodes is most marked in 
those about the root of the lungs, which are frequently of a mottled 
gray or a black color, but it may occur in the mesenteric and other 
nodes. Under similar conditions the diffuse lymphatic structure in 
the lungs and liver may be similarly pigmented. 

Inflammation of the Lymph Nodes with Cheesy Degenera- 
tion. — This lesion of the lymph nodes, which is distinct from the 
above-mentioned comparatively infrequent cheesy degeneration of 
the contents of old abscesses, commences with changes similar to 
those above described in simple inflammation. The node in this con- 
dition is swollen and feels harder than normal ; on section it has 
a uniform reddish-gray color. Microscopical examination reveals a 
great increase in the number of parenchyma cells, some small and 
si3heroidal, others large and polyhedral. Sometimes the larger cells 
are multinuclear, and not infrequently the reticular framework and 
the capsule are thickened. As the process advances the characteris- 
tic necrotic changes make their appearance. We may find at first a 
greater or less number of the cells converted into a strongly refrac- 
tile material, and the nuclei no longer capable of being stained. 
Then larger and smaller masses of cells undergo cheesy degenera- 
tion, with complete destruction of the blood vessels, reticulum, and 
the spheroidal and other cells, and their conversion into a granular 
material. A section through the node in this condition shows the 
cut surface mottled with irregular-shaped, larger and smaller opaque 
white patches, which indicate the areas of cheesy degeneration. 
These patches may increase in size and coalesce, so that a large part 
of, or even the entire gland may be converted into a more or less 
dense, cheesy mass which may be surrounded by the thickened 
capsule. 

In this condition they may remain for a long time, and not infre- 
quently, oAving to the involvement of a series of associated nodes, 
either simultaneous^ or one after another, and the increase of con- 
nective tissue about them, we find large, irregular nodular masses 
made up of a congeries of similarly affected nodes. 

On the other hand, flie clieesv material n\nv soften and break 



430 THE VASCULAR SYSTEM. 

down, and, by the establishment of purulent and necrotic inflamma- 
tion about them, abscesses may form which may open externally. 
These abscesses may heal ; but usually the healing is difficult and 
slow, and long-continued suppurations, frequently with the develop- 
ment of fistulse, are very common. Under these conditions the in- 
flammation may assume a tubercular character. Instead of soften- 
ing, the cheesy material in the glands may become dry and hard and 
undergo calcification. 

Cheesy inflammation of the lymph nodes is most common in the 
cervical, bronchial, and mesenteric groups, but may occur anywhere. 
It is most apt to occur in badly nourished young persons, who, in 
addition to the lesion of the lymph nodes, are very liable to suffer 
from chronic inflammations of the mucous membranes, skin, perios- 
teum, joints, and the subcutaneous and other connective tissues. 
This general condition is known as scrofula, and the lesion of the 
nodes is sometimes called scrofulous inflammation. It is not in- 
frequently associated with tubercular inflammation of the nodes, 
either as an independent lesion or as a part of a general tuberculosis, 
and by some writers tuberculous and scrofulous inflammation of the 
lymph nodes are considered to be identical. In a considerable pro- 
portion of cases, however, of so-called scrofulous inflammation of the 
lymph nodes, there is no formation of tubercle tissue and we find no 
tubercle bacilli, so that we must consider this class of cases as sim- 
ply inflammatory, with a tendency to cheesy degeneration. 

Tubercular Inflammation may occur in connection with simple 
inflammatory changes in the lymph nodes, or with the form of in- 
flammation which tends to cheesy degeneration. It may be local, 
confined to the nodes, or it may occur in connection with general 
acute miliary tuberculosis or with tubercular inflammation of single 
organs. It may occur in single nodes, or in several nodes of the same 
group, or in groups situated in different parts of the body. In its 
simple and acute form there may be no evident change to the naked 
eye in the appearance of the nodes, or they may be besprinkled with 
small, grayish-white, translucent spots. Under these conditions the 
nodes may be reddened and soft, or swollen and denser than normal. 
In more advanced forms of the lesion the tubercles coalesce and un- 
dergo a greater or less degree of cheesy degeneration. Under these 
conditions the cheesy areas are evident to the naked eye as more or 
less sharply circumscribed, opaque, whitish areas, frequently sur- 
rounded by an irregular, more translucent, grayish zone of tubercle 
tissue which merges insensibly into the adjacent tissue. The entire 
node may become involved, and more or less completely converted 
into a cheesy mass, in the periphery of which a zone of tubercle tis- 
sue may or may not be evident. 



THE VASCULAR SYSTEM. 437 

Microscopically the small nodules or railiary tubercles are seen to 
consist of more or less circumscribed collections of small spheroidal, 
or more frequently larger polyhedral cells, with or without well-de- 
fined giant cells. They usually commence to form in the follicles 
and lymph cords of the nodes, and from these may spread and involve 
the entire surrounding tissue. The cheesy degeneration, which here 
as elsewhere is apt first to involve the central portions of the tuber- 
cles, presents the usual appearances. Tubercle bacilli may be found 
in the edges of the cheesy areas or in the tubercle tissue about them. 

Simple inflammatory changes regularly occur in the periphery of 
the tubercles. There is an increase of cells in the lymph sinuses and 
follicles, and a more or less marked swelling, and apparently a pro- 
liferation of the cells of the reticular tissue of the node. In cases in 
Avhich the process is chronic there is often marked increase of the 
connective tissue of the nodes, the reticular tissue becomes dense 
and fibrous, and the trabeculoe and capsule are thickened. The 
tubercles themselves, instead of undergoing cheesy degeneration, 
may become fibrous or be converted into a hyalin material. 

The cheesy material may dry and shrink, and become enclosed 
by a capsule of dense connective tissue and become calcified ; or it 
may soften, and thus cavities be formed in the glands, filled with 
grumous material ; or inflammatory changes may be induced in the 
vicinity of the nodes, leading to abscesses. On the other hand, hy- 
perplastic inflammation in the periphery of the affected nodes may 
result in their becoming bound together into a dense nodular mass. 

When cheesy degeneration has occurred, to the naked e\'e tuber- 
culous lymph nodes may not be distinguishable from those in scrofu- 
lous inflammation, but in some cases the nodular character of the 
new tissue around the cheesy centres is e^^ident. The process is 
usually a slow and chronic one, except when occurring in connection 
with acute miliary tuberculosis in other parts of the body. It may 
occur in any of the nodes, but is most frequent in those of the bron- 
chial, mesenteric, and cervical regions. 

SijphiUtic Inflammation. — The lesions of the lymph nodes 
which occur in connection with syphilitic poisoning vary greatly, 
depending upon the stage of the disease. In the primary stage the 
lymph nodes in the region of the seat of infection are apt to pre- 
sent the lesions of an ordinary acute inflammation, with a tendency 
to the assumption of the purulent form. 

In the secondary stage of the disease the nodes of other regions, 
neck, elbow, axilla, etc., are frecpientl}' swollen and hard. On 
microscopical examination there may be an increase of connective 
tissue in the capsule and trabecuht>, but the chief change is in the 
accumulation in the follicles and lymph sinuses of larger and smaller 



438 THE VASCULAR SYSTEM. 

spheroidal and polyhedral cells. The reticular tissue may be thick- 
ened and the walls of the blood vessels infiltrated with cells. In 
this condition the nodes may remain for a long time, not tending to 
form abscess ; or they may undergo resolution through degenera- 
tion and absorption of the cells. 

In the tertiary stage of the disease the nodes may be the seat of 
chronic inflammation characterized by the formation of gummy 
tumors. Under these conditions they may form large, firm nodular 
masses by the growing together by new connective tissue of several 
altered nodes. The gross and microscopical characters of gummata 
of the lymph nodes are, in the main, similar to those in other parts 
of the body. 

There are important changes in the lymph nodes which occur as 
local manifestations of general diseases, such as tiiphoid fever, 
leprosy, etc., which will be considered under the headings of these 
diseases. 

Degenerative changes in the lymph nodes, with the exception 
of those above described, are not of great frequency or significance. 

Atrophy is a very regular occurrence in old age. In this con- 
dition the nodes are small, hard, and, unless pigmented, white. 
Microscopical examination shows a marked diminution in the num- 
ber of parenchyma cells, while the reticulum and the capsule and 
trabeculse may be thickened. There may be an accumulation of 
fat around the node in connection with senile atrophy. 

It should be remembered, in this connection, that the lymph 
nodes, as well as the lymphatic tissue in general, in children are 
more voluminous and contain a greater number of parenchyma cells 
than in adults. 

Amyloid degeneration of the blood vessels and reticulum of the 
lymph nodes occurs under the conditions which favor this change in 
general. It may occur in connection with amyloid degeneration of 
other parts of the body, or by itself. It may occur in nodes other- 
wise normal, or in those which are the seat of other lesions — thus in 
simple chronic or tubercular inflammation. It is frequently found 
in the mesenteric lymph nodes, in connection with waxy degenera- 
tion of the intestinal mucous membrane. 

Hyalin degeneration of the external layers of the smaller 
arteries and the capillaries of the lymph nodes, and also of the 
parenchyma cells, occurs occasionally in old age or in connection 
with wasting diseases. The vessels and cells are swollen and con- 
verted into a translucent, strongly refractile substance resembling 
amyloid optically, but not responding to its micro-chemical tests. 
By the accumulation of this raaterial the uninvolved parenchyma of 
the nodes may be compressed and atrophied. 



THE VASCULAR SYSTEM. 4:il> 

HYPERPLASIA OP THE LYMPH NODES {Lymphoma). 

In addition to the considerable enlargements of the lym^jh nodes 
in inflammation which have been described above, they become en- 
larged under a variety of conditions which we do not understand. 
This lack of knowledge of the etiology, together with our ignorance 
of the function of the lymph nodes, and the morphological similarity, 
or even identity, which these enlarged nodes present, render it very 
difficult to decide upon the exact nature of the change, and in many 
cases to distinguish one form from another. 

In the first place, there is a class of cases in which, sometimes 
slowly, sometimes with great rapidity, the lymph nodes of certain 
regions, especially the abdominal, axillary, cervical, and inguinal, 
enlarge not infrequently to an enormous extent. They may be 
either hard or soft, even almost fluctuating ; the individual nodes 
may be distinct or merged into one another. Sometimes the nodes 
in nearly all parts of the body are affected. Microscopically we flnd 
that the enlargement is due, in the soft varieties, to an enormous 
increase of small spheroidal and polyhedral cells and a growth of 
the reticular tissue. It is a new formation of lymphatic tissue, but 
the normal relations of follicles, cords, and lymph sinuses are not pre- 
served. In the harder varieties there is a thickening of the reticular 
tissue in addition to an increase of cells. In very rare cases portions 
of the nodes may become cheesy. Sometimes larger and smaller 
haemorrhages occur in the nodes, especially in the softer forms. In 
addition to these changes in the lymph nodes there is, in a consider- 
able proportion of cases, a new formation of lymphatic tissue in 
greater or less quantity in other parts of the body, in the spleen, in 
the gastro-intestinal canal, in the marrow of bones, in the liver, kid- 
neys, etc. , and the number of leucocytes in the blood and in other 
parts of the body is increased. This general condition is known as 
leukcemia and will be considered under the general diseases. The 
enlarged lymph nodes in this disease may be called, for convenience, 
leiikceuiic lynijjhoniata. 

In the second place, there is a form of disease in many respects, 
particularly in the lesion of the lymph nodes, identical with leu- 
kaemia. There is, however, usually a less prominent involvement of 
the spleen and other lymphatic structures, and, what is more strik- 
ing, no increase in the number of leucocytes in the blood. This is 
called Hodgkin's disease, or pseudo-leakcvDu'a, nnd the enlarged 
lymph nodes may in this case be called pseiido-h'iika'nn'c Ii/nipho- 
niata. The lesions of the h^mpli nodes are identical in both diseases, 
and it is convenient to assign ditt'erent names to tliem simply be- 
cause, for reasons which we do not at all understand, thov seem to 



440 THE VASCULAR SYSTEM. 

arise under different conditions and to be associated with a constant 
difference in the character of the blood. 

TUMORS. 

Sarcomata occur in the lymph nodes as primary and second- 
ary tumors, and these may be of various forms : spindle-celled, 
large and small round-celled, and angio-sarcomata. It is not easy 
in many cases to distinguish morphologically between the small 
round-celled sarcomata and the above-described lymphomata. Fi- 
bromata, myxomata, and chondromafa occur in the lymph nodes, 
but are rare. Endotheliomata are described, but are not common. 
Secondary carcinomata are of frequent occurrence, the form of the 
cells and the nature of their growth depending upon the seat and 
character of the primary tumors. 

PARASITES. 

Aside from various forms of bacteria which are not infrequently 
found in the lymph nodes — thus in diphtheria, splenic fever, typhoid 
fever, tuberculosis, etc. — filar ia, trichince, smd pentastomum have 
been described. 



THE ALIMEj^TARY (JAiYAL. 



THE MOUTH. 



MALFORMATIONS. 



Malformations of the lip and cheeks are usually associated with 
defective formation of the bones of the mouth. The entire process is 
generally due to an arrest of development. 

1. The lower jaw is absent ; the upper jaw and hard palate small 
and imperfectly formed ; the temporal bones nearly touch in the 
median line. The lower part of the face is, therefore, wanting ; the 
mouth is absent, or small and closed posteriorly; the tongue is absent. 
Such a malformation is rare ; the foetus is not viable. 

2. The face remains in its early foetal condition of a large cleft : 
the mouth and nose form one cavity ; the orbits may be united in the 
same cavity. The foetus is not viable. 

o. There is a cleft in the upper lip, upper jaw, and hard palate. 
The cleft corresponds to the point of junction of the processes of the 
superior maxilla with the intermaxillary bone. There may be one 
cleft or two, one on either side of the intermaxillary bone. The cleft 
involves the lip alone, or the lip and superior maxilla, or the lip, 
maxilla, and palate. There may be a single or a double cleft in the 
palate, and tlie cleft may involve either the hard or soft palate, or 
both. If there are two clefts of the lip and maxilla the portion of lip 
and bone between them may be small, or entirely absent so as to 
leave a large open space. The soft palate may be entirely absent. 
This is a common malformation and does not endanger life. 

4. Rarely we find a cleft involving the middle of the lower lip, 
and sometimes extending into the inferior maxilla. 

5. Either the inferior, the superior, or both maxillary bones may 
be abnormally small. 

G. The edges of the lips may be partly or completely joined to- 
gether. Tlie opening of the mouth may be only a round hole. 

7. The lips may be absent or imperfectly developed. 

8. The corners of the mouth may be prolonged by clefts in the 
cheeks nearly to the c^ars. 

39 



442 THE ALIMENTARY CAXAL, 

HYPERTEOPHY. 

The skin of the cheeks and lips may be hypertroi^hied in connec- 
tion -with elephantiasis of the face. 

There mar be a thickening of the hps alone, so that they appear 
double. This thickening may be due to an increase of all the ana- 
tomical elements of the hps : or there may be an increase and dilata- 
tion of the hinphatic vessels, gi^-ing to the growth a soft, oedematous 
character. 

IXFLAMMATIOX. 

Catarrhal Stomatitis is found most frequently in children. It 
is produced by a great variety of local and constitutional causes. Of 
the conditions which are seen during life, the congestion, increased 
production of mucus, and swelling of the mucous membrane, but 
httle remains after death. 

During life the congestion and swelhng of the mucous membrane 
are well marked. There are often white patches, produced by the 
death of the superficial epithehal cells. There may be an increased 
production of mucus, which runs constantly from the mouth, or. in- 
stead of this, the entire mucous membrane is unnaturallv drv. 

The only structural changes which can be demonstrated are the 
degenerative changes of the epithehal cells and the production of pus 
globules, which infiltrate to a moderate degree the stroma of the 
mucous membrane and appear on its surface. 

Croupous Stomatitis is produced by local irritants, by extension 
of the same form of inflammation from the pharynx, and it occurs 
with the exanthematous fevers and with diphtheria. 

Portions of the mucous membrane are swollen and congested, and 
covered ^vith a false membrane. This false membrane is composed 
of a thickened layer of epithelium in the condition of coagulation 
necrosis, and of fibrin and pus in variable relative quantity. The 
stroma of the mucous membrane may be infiltrated with pus and 
fibrin, and portions of it may become necrotic. 

STOMATITIS viaCEBO^A^ {Stomacace J Stomatite UJcero-mem 

hraneuse). 

This form of stomatitis occurs in children between the ages of 
four and eight years, and in adults between the ages of eighteen and 
twenty-five years. It is apt to occur in localized epidemics, in hos- 
pitals and asylums, and among soldiers and sailors. Some of the 
forms of mercurial stomatitis seem to be identical with this form of 
inflammation. 

^Bergeron, "Stomatite ulcerosa," Uiiion Medicale, 1859. Bohn, " Mundkrank- 
heiten der Kinder," 1880. 



THE ALIMENTARY CAXAL. 44:> 

The inflammation begins at the margin of the gums of the lower 
jaw. The gums are swollen and coated with a grayish, soft matter 
composed of bacteria and detritus. Then follows destruction of tis- 
sue ; the gums are destroyed around the teeth, and these fall out ; 
the inflammation extends to the lips, cheeks, and tongue. The 
ulcers are coated with a thick, soft, gray membrane. The surround- 
ing soft parts are swollen, and there may be necrosis of the jaws. ^ 

Syphilitic Stomatitis. — As a result of syphilis there may be pro- 
duced either the so-called mucous patches or gummy tumors. In 
the mucous patches we find at first the epithelial layer thickened 
and the papillae of the stroma swollen and infiltrated with cells. 
This may be followed by desquamation of the epithelium and ulce- 
ration of the stroma. 

The deeper gummy tumors may also soften and form ragged 
ulcers of some size. 

Tubercular Stomatitis commences with the formation of miliary 
tubercles or of larger tubercular masses in the stroma of the mucous 
membrane. These masses soon degenerate, soften, and form ragged 
ulcers resembling very closely syphilitic ulcers. 

GANGRENE. 

Gangrene of the lips and cheeks, or noma, is most frequent in ca- 
chectic children as a consequence of the abuse of mercury. Much 
more rarely it occurs in adults after typhus and other exhausting- 
diseases. The disease begins in the mucous membrane of the cheeks 
near one of the corners of the mouth. The mucous membrane be- 
comes black and gangrenous ; the gangrene extends rapidly through 
the entire thickness of the cheek and produces perforation : it ex- 
tends laterally in all directions. 

TUMORS. 

Adenomata are formed in the mucous membrane covering the 
mouth, lips, and soft palate. The tumors are rounded, usually small, 
sometimes as large as a hen's Q^^g. They may be situated in the 
thickness of the mucous membrane, or project iu a polypoid form. 
They are formed by an hypertrophy of the normal mucous glands. 
The glandular acini are increased in number and size, the epithelial 
cells are increased in number and may undergo colloid degeneration. 

Papillomata occur most frequently at the edges of the lips, but 
are also found on. the gums, the floor of the mouth, and the cheeks. 

' i?. 'Volkmann,Y\VQ\\. Arch., Bd. l.,p. 142, describes five cases of iiitlammation 
of the mucous ghmds of the k)wer lip. The lip was swollen and hard, the mucous 
glauds aud their ducts were dilated. 



4:4:4: THE ALIMENTARY CAXAL. 

They are formed of hypertrophied papillce, covered mtli thickened 
epidermis. They very often alcerate. 

Carcinomata are of frequent occurrence. They may be found 
at any part of the mucous membrane of the mouth, but as a rule be- 
gin in the edge of the lower lip. 

They may orginate in an ulcerating papilloma, or as a flat, super- 
ficial growth from the deeper layers of the epithelium, or as deep 
nodules starting in the mucous glands. They are composed of large 
masses of epithelial cells, closely packed together, often formings 
nests, and arranged in anastomosing tubular masses. The stroma 
surrounding these masses is infiltrated with cells. In a few cases 
the infiltration of the stroma with small round cells may be very 
marked, so marked that the epithelial growth may be obscured. 
The new growth increases in size, ulcerates, infiltrates the adjacent 
tissues, and may give rise to metastatic tumors. 

Angiomata are found in the lips. They may be congenital or 
developed after birth. 

Fibromata, lipomata, and enchoudromata have been seen in a 
few cases in the lips. When they appear in the mouth they usually 
grow from the bones. 

THE TOXGUE. 

MALFORMATIONS. 

Absence of the tongue is found in connection with the extreme 
defects of development of the face already mentioned. 

The anterior portion of the tongue may be absent while its base 
remains. The lower jaw is then small. 

The tongue may be partly or completely adherent to the floor of 
the mouth. The frenulum niSLj be abnormally short, or may extend 
to the tip of the tongue. In rare cases the sides of the tongue are 
adherent, or its upper surface may be adherent to the roof of the 
mouth. 

HYPERTROPHY. 

Macroglossia, or hypertrophy of the tongue, is almost always a 
congenital lesion, and is especially common in cretins. The tongue 
is so large that the cavity of the mouth cannot contain it : it is pro- 
truded through the lips and displaces the jaws. The lips may also 
be hypertrophied in the same way. 

There is an hypertrophy of all the anatomical elements which 
make up the tongue, and in addition to this there may be a dilatation 
of the lymphatic vessels. 



THE ALIMENTARY CANAL. 445 



INFLAMMATION, 



Inflammations of the tongue may be associated with similar 
changes in the mouth, or may occur by themselves. 

Superficial Glossitis. — Inflammation involving only the mucous 
membrane of the tongue may occur as an acute or chronic process. 

The acute forms present no marked lesions. 

The chronic forms result in an increased production of epitheliuin 
and an hypertrophy of the papillae of the tongue. 

A moderate development of such an inflammation is not infre- 
quently associated with derangements of the stomach. The tongue 
is large, its surface is irregular from the hypertrophy of the papillae. 
There may be no change in the epithelium, and then the surface of 
the tongue is clean and red ; or the epithelium is increased and the 
tongue is covered with a white fur. 

More severe forms of the disease also occur, especially with 
syphilis. The hypertrophied papillae and increased epithelium then 
alter very decidedly the appearance of the tongue. 

Parenchymatous Glossitis may be produced by mercurial poison- 
ing, by injury, or by unknown causes. The tongue is swollen, the 
muscular and connective portions are congested and infiltrated Avith 
serum and pus. The inflammation may stop at this point or it may 
go on to the formation of an abscess. 

Syphilitic Glossitis. — In persons suffering from constitutional 
syphilis there may be mucous patches on the surface of the tongue : 
or gummy tumors in its stroma, which often soften and form deep 
idcers; or a diffuse, chronic inflammation of the surface of the tongue, 
with hypertrophy of the pa^Dillae. 

Tubercular Glossitis. — There may be a tubercular inflammation 
of the connective tissue of the tongue just beneath the epithelial 
layer, resulting in the formation of tubercle granula and granulation 
tissue. In this way tumors of some little size are formed, which 
may remain unchanged for some time, or may degenerate, soften, 
and form ulcers. 

TUMORS. 

Cysts. — The most common forms of cysts are the sacs beneath or 
partly in the substance of the tongue (ranula). They are formed bv 
dilatation of the ducts of the submaxillary and sublingual glands, or 
make their appearance in the connective tissue beneath and in tlu^ 
tongue. 

Angionia. — Cavernous vascular tumors are found in the sub- 
stance of the tongue and projecting from its surface. 

Lipoma and fibroma are rare. They form nodules in the sub- 
■stance of the tongue or project in a polypoid form. Composite 



44:6 



THE ALIMENTARY CANAL. 



tumors, composed largely of fat, are found in the tongue as a con- 
genital condition. 

Lupus occurs in the form of nodules and ulcers at the base of the 

tongue. 

Sarcomata are rare in this situation. I (Delafield) have seen 
one such tumor in a young child. It formed a nodule as large as a 
chestnut, and was composed of round and fusiform cells. 

Carcinoma. — This form of new growth may begin in the tongue 
or may extend to it from the adjacent tissues. The growth is com- 
posed of large, flat epithelial cells packed closely together in anas- 




Fig. 225.— Section op the Wall of a Cyst op the Neck. 
Formed frora imperfect closure of embryonal gill cleft— diffuse lymphatic tissue. 



tomosing tubular spaces and surrounded by a connective -tissue 
stroma. 

THE PHARYNX AND THE (ESOPHAGUS. 



MALFORMATIONS. 

When, as not infrequently occurs, the embryonal gill clefts do not 
properly close, fistulse may remain. These may in rare cases be com- 
plete, so that an opening exists from the pharynx, larynx, or tra- 
chea to the side of the neck. More frequently, however, these fistu- 
Ise are incomplete and shallow, and open either inward into one of the 
above-named organs or outward on to the neck. Small portions of 
the gill clefts may persist without external openings, and from these 
subcutaneous cysts of the neck are often developed. Or a portion of 



THE ALIMENTARY CANAL. 447 

the cleft may be cut off, forming a cyst, while the fistulas persists 
with its external opening. 

The walls of these fistulae and cysts may be covered with mucous 
membrane having cylindrical or flattened or ciliated surface cells. Or, 
when formed from the outer gill clefts, they may be lined with skin. ^ 

Not infrequently the walls of these cysts and fistulse are emVjed- 
ded in lymphatic tissue which may be diffuse or gathered in nodu- 
lar form (see Figs. 225 and 226). 

The oesophagus may be entirely absent, or its lower portion may 
be present and joined to the pharynx by a solid cord ; or the pha- 
rynx, or the lower part of the oesophagus, may be continuous with, 
the trachea ; or the entire CBSophagus may be represented by a solid 
cord. 




Fig. 226.— Section of the Wall, op a Cyst of the Neck. 
Formed from imperfect closure of embryonal gill cleft— nodules of lymphatic tissue. 

Diverticula of the pharynx, dilatations of the oesophagus, and di- 
vision of the middle portion of the oesophagus into two branches have 
all been observed. 

INFLAMMATION. 

Catarrhal and Croupous Pliaryngitis are usually associated 
with the same forms of inflammation in the mouth and have the 
same characters. 

Ill catarrhal inflammation involving the tonsils and those portions 
of the pharynx richly supplied with the so-called submucous adenoid 
tissue, leucocytes may penetrate in considerable numbers the peculiar 

'Consult Voii Kastanccki and Von ]\Iielecki,y\Yc\\. Airliiv, Bd. cxx.. p. 3S5. 
and Bd. cxxi., pp. 55 and 247. A\so Hartla/, New York :McHHcal Journal, .luly 4th. 
1892. 



448 THE ALIMENTARY CAXAL. 

thin epithelium. ^ These may, on exposed surfaces, form a part of 
the exudate and be removed; or in the crypts of the tonsils they may, 
with epithelium and various forms of bacteria, form tliose whitish 
plugs characteristic of follicular tonsillitis. 

In chronic inflannnation of the tonsils and pharynx there may 
be a large and permanent hyperplasia of the adenoid tissue, with more 
or less dense fibrous tissue, leading to enlargement of the tonsils and 
to' diffuse or circumscribed nodular or pedunculated masses of vas- 
cular new tissue in the vault or elsewhere in the pharjmx. 

Submucous Pharyngitis may occur with inflammations of the 
mucous membrane, ^\dth caries of the cervical vertebrae, with inflam- 
mation of the cervical and j^arotid glands, vnth. periostitis of the 
cranial bones, or may be idiopathic. It may result in swelling and 
oedema, in induration, or in suppuration. It is most important 
when it affects the posterior wall of the pharynx and forms retro- 
pharyngeal abscesses. Sucli abscesses may cause death by suffo- 
cation. 

Catarrhal Qilsophagitis may be either acute or chronic. The 
chronic form may produce ulceration, or relaxation and dilatation of 
the walls, or hypertrophy of the muscular coat. 

Croupous CEsophagitis is found "with croup of the pharynx, and 
after the exanthemata and other severe diseases. 

Irritating and caustic acids and alkalies destroy larger or smaller 
portions of the mucous membrane. The necrosed portions are of a 
black or whitish color, surrounded by a zone of intense congestion. 
If the patient recover the patches of membrane which have been 
destroyed slough, fall off, and leave a granulating surface. In this 
way dangerous stenosis of the oesophagus may be produced. 

Foreign bodies which are swallowed and become fixed in the oeso- 
phagus cause inflammation of the mucous membrane and of the ad- 
joining soft parts. The inflammation may go on to produce ab- 
scesses around the oesophagus, or to destroy the wall of the canal, 
and the foreign body finds its way into the trachea, aorta, or peri- 
cardium. 

Inflammation of the submucous tissue of the oesoi^hagus. apart 
from the cases just mentioned, is not common. It may cause the 
formation of abscesses, or of fibrous tissue, which may produce 
stenosis. 

ULCERATIOX. 

Ulceration of the pharynx occurs in rare cases as the result of 
catarrhal inflammation. More frequently it is produced by syphilis, 

^See Rodenpyl. "Anatomy and Physiology of the Faucial Tonsils, " Am. Jour. 
Med. Sciences, March, 1891. 



THE ALIMENTARY CANAL. 4+0 

either in the form of superficial ulcers or of deep and extensive de- 
structions of tissue from the softenini^ of gummy tumors. 

Lupus also sometimes attacks the upper part of the pliarynx 
and produces extensive ulceration. Ulceration of the cjesophagus is 
not common, but a few cases of simple perforating ulcers have been 
described. ' 

Foreign bodies in the oesophagus may perforate its wall, as al- 
ready mentioned. Perforation of the oesophagus from without may 
be jjroduced by inflamed bronchial glands, by cavities and gangrene 
of the lungs, by abscesses in the mediastinum, by abscesses ac- 
companying caries of the vertebrae, and by aneurisms of the aorta. 
Cases have been described of rupture of the wall of the oesophagus 
by violent coughing and vomiting, but it seems probable that there 
was really some pre^dous disease to account for the rupture. 

DILATATION." 

Simple cylindrical dilatation of the oesophagus is usually the re- 
sult of long-continued stenosis of the oesophagus or of the cardiac 
end of the stomach, although not nearly all the stenoses are fol- 
lowed by dilatation. These dilatations are forined at first immedi- 
ately above the stenosis and then extend upward. Only in rare cases 
does the dilatation involve the whole length of the tube. The entire 
wall of the dilated portion of the oesophagus is thickened, and there 
may be polypoid growths from the mucous membrane. 

In rare cases there is cylindrical dilatation of part or of the whole 
of the oesophagus without a stenosis or any discoverable cause. In 
these cases the dilatation is usually greatest near the middle of the 
oesophagus and diminishes upward and downward, so that the oeso- 
phagus has a fusiform shape. The dilatation may reach a very con- 
siderable degree, the walls of the oesophagus are thickened, its 
mucous membrane may be covered with papillary outgrowths or 
ulcerated. 

The Sacculated Dilatations of the oesophagus are of two kinds : 
those due to pressure, and those due to traction. 

The dilatations due to pressure are situated in the posterior wall 
of the pharynx, just at its junction with the oesophagus. The 
smaller sacs are from the size of a pea to that of a hazelnut ; the 
larger sacs may reach an enormous size and hang down between the 
oesophagus and the vertebral column, the opening into the cesopha- 
gus remaining comparatively small. It is supposed that a limited 



^ Omefe a. Walthcr, Sowv. fiir Chir. luul Auii-eiiheilk., IM. xix. Mtvl. Chir. 
"Trans., vol. xxxvi. Rokitansky, " Path. Auat." 

^ Ziemssen, '• Cyclopiudia of Medicine," viii., p. 47. 



450 THE ALIMENTARY CANAL. 

■area of the wall of the oesophagus loses its power of resistance against 
the pressure exercised upon it in each act of swallowing ; it then is 
forced outward by the pressure, and so there is formed first a protru- 
sion and then a sac. When a sac is formed the food enters it, accu- 
mulates there, and so the sac becomes larger and larger. 

The dilatations due to traction are situated on the anterior wall of 
the oesophagus, at a point nearly corresponding to the bifurcation of 
the trachea. They are of funnel shape, mth the small end outward. 
Their length varies from two to twelve millimetres ; the width of the 
opening into the oesophagus is from six to eight millimetres. 

These dilatations are due to inflammation of the parts adjoining 
the oesophagus, especially of the bronchial glands, followed by ad- 
hesions to some part of the anterior wall of the oesophagus. These 
adhesions then contract and draw the wall of the oesophagus out- 
v/ard, and in this way the dilatations are formed. 

At a later time these sacs may perforate into the bronchi, the 
lungs, the pleural cavity, the pericardium, the aorta or pulmonary 
artery. 

STENOSIS. 

Congenital Stenosis. — Besides the defects of development of the 
oesophagus which are incompatible with life, there may be a congen- 
ital stenosis of some part of it which causes difficulty in swallowing, 
but yet does not destroy life. 

Stenosis by Compression is not uncommon. Tumors of the 
neck and mediastinum, and aneurisms of the aorta, are the usual 
causes. 

Stenosis by Obstruction. — Foreign bodies may be lodged in the 
oesophagus. Tumors may hang down from the pharynx into the 
oesophagus, or may be situated in the wall of the oesophagus. In- 
flammation of the oesophagus, due to the ingestion of irritating poi- 
sons, produces cicatricial stenoses. A few cases of stenosis due to 
syphilitic inflammation have been reported. 

TUMORS. 

The veins of the oesophagus may be enormously dilated. They 
may rupture and so give rise to hsemorrhage. ^ 

Cysts. — Small retention cysts of the follicles of the mucous mem- 
brane are sometimes found. Yan Wyss" describes a cyst, as large as 
an apple, attached to the posterior wall of the oesophagus one and 
one-half inches above the stomach. It was filled with ciliated epi- 
thelium. 

^ Brisioioe, Trans. London Path. Soc, 1856. 
-Virch. Arch., Bd. li., p. 143. 



THE ALIMENTARY CANAL. 



4ol 



Papilloniata of small size may be found in considtiraljle num- 
bers throughout the entire length of the oesophagus, or may occur 
singly. Large papillary tumors are more rare. 

Fibromata grow from the periosteum of the bones at the base of 
the skull, and project into the cavity of the pharynx and posterior 
nares in the form of large polypoid tumors. Small fibrous tumors 
are formed in the submucous connective tissue of the oesophagus. 
Tumors, which attain a very large size, originate in the submucous 




Fig. :^27.— Adenoid Polyp of Pharynx. 

connective tissue on the anterior wall of the lower part of the pha- 
rynx, and as they grow hang down into the oesophagus. Sc^f t poly- 
poid tumors consisting largely of loose succulent connective tissue 
and lymphatic tissue are often called 'Sidenoid polyps" (see Fig. •>?•>?:). 

Lipomata of small size are sometimes found in the wall of the 
oesophagus. 

Mijoniata composed of smooth muscle may grow in t\\o nuistni- 
lar coat of the oesophagus and attain a considerable size.' 

' Vircli. Arcli., Bd. xliii., p. 137. Med. Times and Gazette, Novombor OStli. 1S74. 
Glasgow ]\red. Jourual, February. 1873. 



452 



THE ALIMENTARY CANAL. 



Adenoma. — A polypoid adenoma composed of tubules lined with 
cylindrical epithelium, and growing from the anterior wall of the 
oesophagus, has been described by Weigert/ 

I (Delafield) have seen one tumor, the size of a chestnut, growing 
in the soft palate, Avhich was composed of a stroma of connective and 
mucous tissue in which were irregular, anastomosing tubules filled, 
with small, polygonal, nucleated cells. It could be called an adenoma 
or a carcinoma. 

Another composite tumor grew from the mucous membrane of the 
pharynx behind the left tonsil. It filled the pharynx below the level 



V o V 






-'I 

l 



Jll 






e 



i 



^ ) 



Fig. 228.— Diffuse Sarcoma ok the Pharynx, X 850 and reduced . 

of the palate. It had the gross appearance of a myxo-sarcoma, the 
central portions being very soft. It was composed of connective 
tissue, mucous tissue, fat, sarcomatous tissue, and irregular tubules 
lined with small, polygonal, epithelial cells. Some of the tubules were 
distended with masses of hyalin matter. The whole structure re- 
sembled that of the tumors so often found in the parotid region — 
tumors which can be called '' adenoid myxo-sarcomata.^' 

Carcinomata may originate at any part of the wall of the 
pharynx and oesophagus. They are composed of flat epithehal cells 
closely packed together in masses in the usual way. In the oeso- 

^ Yircli. Arch., Bd. Ixvii., p. 516. 



THE ALIMENTARY CANAL. 4o^> 

phagiis the new growth begins in the deeper layers of the mucous 
membrane, and grows so as to encircle the tube for a length of one 
or more inches. The tumor remains as a flat infiltration, or it ulcer- 
ates, or it projects inward in large, fungous masses. The growth 
may extend up and down the oesophagus, and even involve the 
pharynx or stomach. 

The ulcerative process may extend outward so as to produce perfo- 
ration into the air passages, the lungs, pleurse, pericardium, and large 
blood vessels. 

The new growth may extend outward and infiltrate the surround- 
ing soft parts, so that the oesophagus is surrounded by large, solid, 
cancerous masses. Metastatic tumors are also sometimes formed. 

Sarcoma. — I have seen one case in which there was a diffuse growth 
involving both the tonsils, the posterior and lateral walls of the 
pharynx, the base of the tongue, and the epiglottis. The new growth 
replaced the mucous membrane, infiltrated the soft parts for a short 
distance, and projected inward in polypoid masses. It was composed 
of small, polygonal, nucleated cells contained in a very delicate 
nucleated stroma^ (Fig. 228). 

THE STOMACH. 
MALFORMATIONS. 

Malformations of the stomach are not common. The or^-an mav 
be entirely wanting in acephalous foetuses. It may be of various de- 
grees of smallness, sometimes no larger than the duodenum. It may 
be divided into two halves by a deep constriction in the middle. The 
pyloric orifice may be stenosed or entirely closed. The stomach may 
be outside of the abdominal cavity from a hernial protrusion through 
the diaphragm or at some point in the abdominal wall. It is found 
on the right side, instead of the left, when the other \nscera are 
transposed, and the position of the cardiac and pyloric orifices is 
correspondingly inverted. 

POST-MORTEM CHANGES. 

In adults the stomach after death is of a grayish or pinkish color, 
sometimes mottled with red ecchymoses. The mucous membrane is 
soft and the epithelium easilv brushed off. At the fundus the food is 
usually found collected, and here the mucous membrane is the softest. 
It is very connnon to find the epithelium removed from the entire 
fundus of the stomach, so that all that portion of its wall is grayer 

' For literature of nialiiiiiant disease of the tousils, cousult Newman, American 
Journal of the 3Iedical Scieuces, 3Iav, 1S03. 



454 THE ALIMENTARY CANAL. 

and thinner, there being a sharp dividing line between the two por- 
tions. Sometimes this post-mortem softening process goes on to de- 
stroy all the coats of the stomach, and even the adjoining portion of 
the diaphragm. In this way the contents of the stomach may be 
emptied into the pleural cavity by a large, ragged opening in the 
stomach and diaphragm. When the softening affects all the coats of 
the stomach the softened portion is not sharply limited. The entire 
thickness of the affected portion of the wall is converted into a gray 
or yellow semi-transparent jelly, or into a blackish, broken-down pulp. 

This softening is most frequent in children, but also occurs in 
adults, usually in connection with severe and exhausting diseases. 

A similar post-mortem softening of the wall of the oesophagus 
has been described by Moxon. ^ 

INJURIES. 

Perforating wounds of the stomach usually give rise to a fatal 
peritonitis. It is possible, however, for the wound to heal, or a gas- 
tric fistula may be forined. 

Rupture of the stomach may be produced by severe blows or falls. 

HAEMORRHAGE. 

Small extravasations of blood in the wall of the stomach are fre- 
quently found in persons who have died from one of the infectious 
diseases. 

Haemorrhage into the cavity of the stomach may be produced in 
a variety of ways. 

In ulcers of the stomach there ixiay be bleeding from the small 
vessels of the ulcer or from the perforation of a larger artery. 

In cancer of the stomach there may be bleeding from the tumor. 

Some cases of chronic gastritis are characterized by general bleed- 
ing from the mucous membranes of the stomach. 

Cirrhosis of the liver is not infrequently attended with large 
haemorrhages from the mucous membrane of the stomach. 

Small aneurisms of the arteries in the wall of the stomach may 
rupture internally. 

In yellow fever and some of the other infectious diseases there is 
haemorrhage into the cavity of the stomach. 

Patients may vomit b'xood during life, and after death no lesion to 
account for the bleeding be found. 

INFLAMMATION. 

Acute Catarrhal Gastritis, as we see it after death, is usually 
1 Trans. Lond. Path. Soc, 1870, p. 159. 



THE altmp:ntary caxal. loo 

due to the ingestion of irritating substances, or forms part of the 
lesions of cholera morbus. If we can judge from clinical symptoms, 
it occurs during life as a temporary condition from a variety of causes. 

After death the mucous membrane is found congested and swollen, 
or the congestion may have disappeared. The mucous membrane is- 
coated with an increased amount of mucus, especially at the p3'loric 
end of the stomach. Sometimes there are a number of minute white 
dots in the substance of the mucous membrane. 

The structural changes in the mucous membrane consist simply 
in a swelling of the cells of the gastric tubules, a slight infiltration 
of the stroma with pus cells, and a swelling of the patches of lym- 
phatic cells. The little white dots, when they are present, are com- 
posed of small foci of pus between the gastric tubules, with degene- 
ration and destruction of some of the tubules. 

Chronic Catarrhal Gastritis is a very common disease. There 
is, however, no very close relation between the severity of the symp- 
toms during life and the extent of the lesions found after death. 

In some cases chronic alcoholism, or the abuse of drugs, or the 
mode of life of the patient seems to be the cause of the lesion. 
Chronic phthisis, chronic B right's disease, cirrhosis of the liver, and 
fatty liver are often accompanied by chronic gastritis. Organic dis- 
ease of the heart, or pressure on the ascending vena cava, produces a 
form of chronic gastritis characterized by intense general congestion. 

After death the stomach is found either empty or still containing 
food. It is of normal size, or dilated, or small, sometimes hardly 
larger than the duodenum. Its inner surface is coated with a thick 
layer of tenacious mucus, most abundant at its pyloric end. The 
mucous membrane is congested, or white, or slate-colored, or mottled 
with small white spots. It is of normal thickness, or thinned, or 
thickened, or there are little polypoid projections from its surface, or 
there is cystic dilatation of the gastric tubules. The connective tissue 
and muscular coats remain unchanged, or the}' are thinned and re- 
laxed, or they are h^-pertrophied. The hypertrophy may be diffuse, 
or it is confined to the pyloric end of the stomach and may then 
produce stenosis of the pylorus. 

The minute lesions consist principally in changes in the mucous 
membrane. The cells of the gastric tubules are swollen, degenerated, 
and broken down. The tubules are atrophied and deformed, or di- 
lated into cysts. The patches of lymphatic tissue about the blind 
ends of the tubules are increased in size. The connective tissue be- 
tween the tubules is infiltrated with cells and increased in cpiantity. 
Croupous Gastritis is of rare occurrence. It is found in chil- 
dren with croupous inflannnation of the pharynx and cvsopliagus, 
and is then usually in small patches. In adults it is almost ahvays 



45G THE ALIMENTARY CAXAL. 

secondary to typhus, j^yaeniia. puer^Deral fever, cholera, dysentery, the 
exanthemata, and irritatmg poisons. The false membrane is in 
small patches, or may line a large part of the stomach. The disease 
is usually not diagnosticated during hfe, the symj^toms of the pri- 
mary disease diverting attention from the gastritis. 

I (Delafield) have seen one case of idiopathic croupous gastritis in 
an adult. A man, forty-six years old, was in good health until eight 
days before his death. At that time he caught cold, had pains over 
his bowels, tenderness over the hver, constipation, cough with mu- 
cous expectoration, temperature lO'H", 2^ulse l'2u. On the day of his 
death, the eighth day of the disease, the temperature was 100°, j^ulse 
112, tongue dry, abdomen t^inpanitic and tender, and he died in a 
l^rolonged attack of sjTicope. At the autopsy all the viscera were ex- 
amined. ExcejDting e^udences of bronchitis in the lungs, there were 
no lesions save in the stomach. About two-thirds of the internal 
surface of the stomach, including the lesser curvature and anterior 
and posterior walls, appeared to be covered with a thick false mem- 
brane, wliich did not qitite reach to the cardiac or pyloric orifices. 
Minute examination showed that there was a layer of exudation on 
the internal surface of the mucous membrane. This exudation con- 
sisted of fibrillated fibrin and lymphoid cells dipping into the mouths 
of the follicles. Beneath the exudation the mucous membrane was 
thickened and altered. A large nimiber of lymphoid cells separated 
the follicles, and even replaced them entirely. The submucous layer 
was very much thickened by the presence of lymphoid cells, fibril- 
lated fibrin, and fibrous tissue. The muscular coat was separated 
into layers by groujDS of lymphoid cells. 

Wilks and IMoxon ' mention a similar case in a man with chronic 
Brighfs disease, and a case of both croupous gastritis and cohtis 
^vith abscess of liver. 

Suppuratife or Phlegmonous Gastritis. — A formation of cir- 
cumscribed collections of pus may occur in the connective-tissue coat 
of the stomach, as it does in other i^arts of the body, in puerperal 
fever and the infectious diseases. 

Idiopathic suppurative . gastritis is a disease of rare occurrence. 
Leube" has collected thirty- one cases, of which twenty-six were 
males and five females. In some of the cases the infiammation was 
ascribed to the excessive use of alcohol, in others to a wound in the 
region of the stomach, in others to some error in diet. 

Fagge ^ describes a case in a male of fif tj^-one years of age, with- 
out discoverable cause. 

' "Path. Anat.," p. 381. 

^ Leube, '' Ziemssen's Cyclopaedia," vii., p. 157. 

=^ Trans. Lond. Path. Soc, 1875, p. 81. 



THE ALIMENTARY CANAL. 457 

Silcock ' describes a case in which the gastritis followed the ope- 
ration of gastrostomy. 

I have seen one case occurring in an adult male, without any 
known cause. 

The suppurative inflammation seems to begin in the connective- 
tissue coat of the stomach. From thence it may extend to the glan- 
dular coat and produce perforations, or outward to the muscular and 
peritoneal coats. In some cases there is added a local or general 
peritonitis. 

The inflammation may involve one or more circumscribed areas 
and so produce abscesses, or it may be a diffuse process involving 
the whole extent of the wall of the stomach. 

Toxic Gastritis. — The mineral acids, the caustic alkalies, arse- 
nic, corrosive sublimate, and the metallic salts, phosphorus, camphor, 
and all other irritating materials, cause different lesions of the 
stomach, according to their quantity, their strength, and the length 
of time that has elapsed before death. 

In large quantities they destroy and convert into a soft, blackened 
mass both the mucous membrane and the other coats, so that perfo- 
ration may take place. In smaller quantities they produce black or 
white sloughs of the mucous membrane, surrounded by a zone of in- 
tense congestion. If death does not soon ensue the ulcerative and ' 
cicatricial processes which follow such sloughs may contract and 
deform the stomach in various ways. 

If the poisons are of less strength they produce a diffused con- 
gestion of the mucous membrane, with catarrhal or croupous exuda- 
tion on its surface and serous infiltration of the submucous coat (see 
chapter on Poisons). 

ULCERS OF THE STOMACH. 

. The Chronic Perforating Ulcer. — This form of ulcer is often 
seen ; according to Brinton, in five per cent of persons d^-ing from 
all causes. It occurs in females nearly twice as frequently as in 
males. As regards the age, Brinton concludes that the liability of an 
individual to become the subject of gastric ulcer gradually rises, 
from what is nearly a zero at the age of ten, to a high rate, which it 
maintains through the period of middle life ; at the end of which 
period it again ascends, to reach its maximum at the extreme age of 
ninety. Lebert gives one hundred and ninety-eight c<^ses in which 
the ulcers were found at the autopsy, as follows : 



^ Trans. Lond. Path.Soc, 1888, p. 90. 
40 



458 



THE ALIMENTARY CANAL. 



AGE. 



15 to 20 years, 
20 to 30 years, 
30 to 40 years, 
40 to 50 years, 



NUMBER OF CASES. 



20 
48 
28 
43 



AGE. 



50 to 60 years 
60 to 70 years 
70 to 80 years 



NUMBER OF CASES. 



29 

19 

5 



Hauser^ gives thirty autopsies from Erlangen of ulcers which 
were still open, as follows : 



AGE. 



20 to 30 years 
30 to 40 years 
40 to 50 years. 



NUMBER OF CASES. 



AGE. 



50 to 60 years, 
60 to 70 years, 
70 to 80 years 



NUMBER OF CASES. 



Moore"^ gives the following table of the fatal cases of ulcer of the 
stomach occurring at St. Bartholomew's Hospital from 1867 to 1879: 



SEX. 



M. 
M. 
M. 
M. 
M. 
M. 
M. 
F. 
M. 
M. 
M. 
F. 




POSITION. 

Near pylorus 

Greater curve near pylorus, 

Near pylorus 

Pylorus 

a 

Lesser curve near pylorus . . 

Cardiac end , 

Near pylorus , 

Posterior vrall. . . . , 



CAUSE OF DEATH. 



Perforation. 
Haemorrhage. 
Exhaustion. 
Phthisis. 

Exhaustion. 

Perforation. 

"^inus in liver to lung. 

Haemorrhage. 

Perforation. 



Goodhardt^ describes an ulcer of the stomach, which proved fatal, 
from haemorrhage in an infant at birth. 

The situation of these ulcers, according to Brinton, is as follows : 
In 43 per cent, the posterior surface ; in 27, the lesser curvature ; in 
16, the pyloric extremity ; in 6, both the anterior and posterior sur- 
faces ; in 5, the anterior surface only ; in 2, the greater curvature ; 
in 2, the cardiac pouch. Thus about 86 ulcers in every 100 occupy 
the posterior surface, the lesser curvature, and the pyloric sac. 

As regards the number of ulcers, two or more are present in about 
twenty -one per cent; there maybe two, three, four, or even fii-e 
ulcers. In cases of multiple ulcers the ulcers are often developed 
successively. 

In size the ulcers vary from one-quarter of an inch to five or six 
inches. 

1 " Das chron. Magengesch., 1883." ^ Trans. Lond. Path. Soc, 1880, p. 110. 

•Ibid., 1881, p. 79. 



THE ALIMENTARY CANAL. 459 

They are usually of circular shape, sometimes oval ; sometimes 
two or more are fused together. 

The perforation is largest in the mucous membrane. It may re- 
main confined to this, cr extend outward and involve the connective 
tissue, muscular and peritoneal coats, its diameter becoming smaller 
as it advances. The ulcer looks like a clean hole punched out of the 
wall of the stomach. Its floor shows no active inflammatory changes. 
Its edges may be in the same condition, or they may be thickened by 
the growth of connective tissue and cells. The rest of the mucous 
membrane of the stomach is apt to be in a condition of chronic ca- 
tarrhal inflammation. 

The ulcer may perforate directly through the wall of the stomach, 
and the contents of the latter are discharged into the peritoneal cav- 
ity ; or adhesions are formed between the wall of the stomach and 
the neighboring viscera, so that the bottom of the ulcer is closed ; or 
if the liver, the intestines, or the abdominal wall become adherent, 
they may be invaded by the ulcerative process, and ca\dties or fistu- 
IsB are formed communicating with the stomach ; or, if the adhe- 
sions are incomplete, a local peritonitis and collections of pus may be 
developed. 

During the progress of the ulcer there may be repeated small 
haemorrhages from the erosion of small blood vessels, or large haem- 
orrhages from the erosion of large arteries. 

In manv cases these ulcers cicatrize, and such a cicatrization mav 
produce various deformities of the stomach. 

It is very difficult to understand how these ulcers are j^roduced. 
It seems probable that the nutrition of a circumscribed part of the 
wall of the stomach is interfered with, and that this portion is then 
destroyed by the action of the gastric juice. But we are still igno- 
rant of the waj in which the obliteration of the arteries is effected. 
It has, indeed, been demonstrated in animals that an artificial em- 
bolism of the branches of the gastric arteries will produce ulcers of 
the stomach ; and in the human stomach we occasionall}' meet \di\\ 
cases of embolism of the branches of the gastric artery and ulcers. 
But the clinical histor}^ of most cases of ulcer of the stomach will 
not correspond with such a method of causation. A chronic oblite- 
rating endarteritis would seem to be a more probable cause. 

Hcemorrhagic Erosions occur as rounded spots or narrow 
streaks, formed by a loss of substance of the mucous membrane. 
The mucous membrane at these points is congested, soft, and co\-- 
ered by small blood clots. The destruction of the mucous mem- 
brane is usually superficial, but may involve its entire thickness. 
The number of these erosions mav be so great that the entire inter- 
nal surface of the stomach is studded with them. Thev Liive rise to 



460 THE ALIMENTARY CANAL. 

repeated hsemorrhages, and are accompanied by catarrhal inflam- 
mation of the rest of the mucous membrane. 

They occur at all periods of life, even in infants. Their usual 
seat is the pyloric portion of the stomach. 

They may be idiopathic. Usually, however, they occur in con- 
nection with some serious general disease. 

Follicular Ulcers somewhat resembling the ulcers of the small 
intestine are occasionally met with. They are produced by changes 
in the aggregations of lymphatic tissue which are situated about the 
blind ends of the gastric tubules. 

DILATATION. 

Very considerable degrees of dilatation of the stomach are found 
at autopsies, without stenosis of the pylorus or any other mechanical 
cause to account for them. It is usually diflicult to determine how 
long these dilatations have existed and how much effect they have 
in causing death. Mne such cases are recorded by Goodhardt. ^ 

Acute Dilatation of the stomach, with vomiting of very large 
quantities of thin fluid, has been observed in a few cases. ^ It is a 
very curious condition, the dilatation of the stomach being developed 
suddenly and without discoverable cause. 

Of the mechanical causes which produce dilatation of the stom- 
ach, stenosis of the pylorus is the most common. Such a stenosis 
may be effected by a tumor, by chronic inflammation and thicken- 
ing, and by the cicatrization of ulcers. Less frequently obstructions 
of the small and large intestines act in the same way. 

Some forms of chronic gastritis are attended with dilatation of 
the stomach without stenosis. 

In rare cases circumscribed, sacculated dilatations are produced 
by the presence of foreign bodies — portions of wood, metal, etc. 

TUMORS. 

Papilloma. — It has already been mentioned that in some cases 
of chronic gastritis there are small, polypoid hypertrophies of the 
mucous membrane. Besides these we find polypoid tumors which 
may reach a considerable size. They are composed of a connective- 
tissue stroma arranged so as to form tufts covered with cylindrical 
epithelium. In some cases there are also tubules lined with cylin- 
drical epithelium, so that the tumor has partly the structure of an 

^ Trans. Lond. Path. Soc, 1883, p. 88. 

2 Ibid., vol. iv. and vol. xxxiv., p. 82. Rughes Bennett, " Practice of Medicine." 
Fagge, Guy's Hospital Reports, vol. xviii., p. 1. Andral, Clinique Medicale. 



THE ALIMENTARY CANAL. 401 

adenoma. Fibromata of small size are sometimes found in the con- 
nective-tissue coat. Lipomata are formed in the submucous con- 
nective tissue in the shape of rounded or polypoid tumors. They 
usually project inward, but sometimes outward beneath the perito- 
neum. They may also appear in the form of numerous yellow nod- 
ules beneath the mucous membrane. 

Myomata occur in the form of rounded tumors which originate 
in the muscular coat, but may gradually separate themselves from it 
and project inward or outward. The submucous myomata are at 
first small tumors lying loosely attached in the submucous tissue. 
As they grow larger they push the mucous membrane inward and 
take the shape of polypoid tumors. Lymphomata in the wall of the 
stomach are seen in some cases of leukaemia. 

Sarcomata are said to occur in the wall of the stomach in rare in- 
stances. It must be admitted that in some of the tumors of the wall 
of the stomach, which are ordinarily called cancerous, the structure 
is not well defined, and it is possible that some of them are sarco- 
mata. 

A myo-sarcoma growing outward from the greater curvature of 
the stomach is described by Brodowski. ' The tumor weighed twelve 
pounds. It was composed largely of smooth muscle cells. There 
was a secondary tumor in the liver. 

Adenoma, — It has been already mentioned that in some of the 
papillary tumors of the mucous membrane there is a considerable 
growth of tubules lined with cylindrical epithelium. 

Besides these we find in the submucous coat circumscribed tumors 
composed of tubules like those of the gastric mucous membrane. 

Small tumors resembling the pancreas have also been seen in the 
submucous and subserous coats. 

Carcinoma of the stomach is almost always primary. But very 
few secondary cases have been recorded. " 

Primary carcinoma of the stomach is of the colloid varietv, or 
common cancer, or cancer with cylindrical epithelial cells, or it is pig- 
mented. 

Colloid cancer is composed of a connective-tissue stroma, arranged 
so as to form cavities of different sizes, which contain colloid matter 
and polygonal cells. It infiltrates first the submticous connective 
tissue and then extends inward and outward. In this way there is 
formed a diffuse thickening of the pyloric end of the stomach rather 
than a "circumscribed tumor. Sometimes the whole of the wall of the 
stomach is changed in this way. Secondary tumors are usually situat- 
ed in the peritoneum. 

1 Virch. Arch., Bd. Ixvii., p. 227. 

'Ibid., Bd. xxxviii. and Ixxxvi., p. IT)!). Tnuis. Path. Soc, London. ISTO. p. 20 i. 



462 THE ALIMENTARY CANAL. 

Carcinoma with cylindrical epithelial cells. These tumors are 
formed of a connective-tissue stroma, which may contain numerous 
round cells, and of tubules lined with cylindrical epithelium hke that 
of the mucous membrane of the stomach. In these tumors the new 
growth seems to begin in the gastric tubules. As the arrangement 
of the tubules is more or less regular, these tumors may be called 
adenomata or carcinomata (see Fig. 129). 

Common cancer is formed of a connective-tissue stroma enclosing 
rounded and tubular spaces filled with small, polygonal, nucleated 
cells. In some cases this structure is well marked. In others the 
stroma is abundant and filled with round cells, the spaces are very 
small, and the epithelial cells few ; it may then be difficult to distin- 
guish between inflammatory thickening, sarcoma, and carcinoma. 

Both these forms of carcinoma, common cancer and cancer with 
cylindrical cells, run the same course as regards their gross appear- 
ance, their situation, and their development of metastatic tumors. 

About sixty per cent of these tumors are situated at the pyloric 
end of the stomach, on the lesser curvature or on the posterior wall. 
The cardiac end of the stomach, the greater curvature, or nearly the 
entire wall of the stomach may also be the seats of the new growth, 
but not as frequently. 

The new growth usually follows one or other of three types. 

1. There is a circumscribed, flat tumor formed in the deeper 
layers of the mucous membrane and pushing this membrane inward. 
After a time the mucous membrane over the centre of the tumor 
dies, the destructive process involves the tumor also, and so an ulcer 
with thickened edges is formed. In some cases the new growth ex- 
tends laterally and outward, while the central destruction still con- 
tinues ; then the ulcers reach a large size, their walls and floor are 
thick, and peritoneal adhesions are formed over them. In other cases 
the ulcer perforates completely through the wall of the stomach, un- 
less the opening is closed by adhesions to the neighboring, viscera. 

2. Large rounded tumors are formed, often several inches in dia- 
meter, which project into the cavity of the stomach. 

3. There is a diffuse, flat infiltration of the deep layers of the mu- 
cous coat, of the connective-tissue coat, and sometimes of the muscu- 
lar coat, which does not ulcerate and hardly forms a tumor. This 
infiltration may be confined to the pyloric end of the stomach, or 
may involve nearly the whole of its wall. 

There is in most of the cases a good deal of chronic catarrhal in- 
flammation of the mucous membrane. 

If the pylorus is obstructed the stomach is often dilated. 

The new growth may extend from the stomach to the oesophagus, 
but it very seldom involves the duodenum. 



THE ALIMENTARY CANAL. 4G3 

Metastatic tumors are very common. The liver, the lymph. itic 
glands, and the peritoneum are the parts most frequently affected, 
but such metastases have been seen in nearly every part of the body. 

DEGENERATIONS. 

Calcification of the mucous membra^ne of the stomach some- 
times occurs as a metastatic process in connection with extensive 
diseases of the bones. 

Waxy Degeneration sometimes involves the blood vessels of the 
mucous membrane. 

THE INTESTINES. 
MALFORMATIONS. 

Diverticula of the intestines occur in several different wavs : 

1. The abdominal walls are cleft asunder at the navel. The ileum 
opens through this cleft by a narrow aperture in its wall. The lower 
portions of the ileum and the colon are small or entirely closed. 

2. There is an opening in the abdominal wall as before, but there 
is not a direct opening into the ileum. There is a long diverticulum 
of the ileum, with an open end projecting into the opening in the ab- 
dominal wall. 

3. The abdominal wall is closed. There is a diverticulum of the 
ileum, connected with the navel by a solid cord. 

4. There is an unattached diverticulum of the intestine. This is 
much the most common form. The diverticula occur only in the 
lower part of the ileum. They usually spring from the convex sur- 
face of the intestine, more rarely from its attached border. In the 
latter case they are joined to the mesentery by a fold of peritoneum. 
The diverticulum forms a pouch, one to six inches long, of about the 
same diameter as the intestine, smallest at its free extremitv. 

Such diverticula do not interfere with the functions of the intes- 
tines. They sometimes form part of a hernia. Sometimes the remains 
of these intestinal diverticula — called Meckel's diverticula — form soft, 
projecting tumors at the umbilicus in children. Microscopical exam- 
ination of such tumors often shows the structure of the intestinal 
mucosa and muscularis. If they remain attached by a tibrous cord 
to the navel, this cord may be the cause of incarceration of a portion 
of the intestines. 

CloaCciB consist in the union of the rectum, bladder, ;itu1 organs of 
generation in a common outlet. 

1. Simple Cloacae are : (a) Complete, and consist in the common 
opening of the urethra or ureters, tlie vaL;-ina. and tho rectum into 



464 THE ALIMENTARY CANAL. 

the closed bladder, or into a sinus opening outward which represents 
either the vagina or the rectum. (6) Incomplete. The rectum opens 
into the vagina, the bladder, or the urethra, while the lower part of 
the rectum is closed or absent. 

2. Cloacce combined with Cleft Bladder. — (a) The simple cleav- 
age of the intestines is combined with cleft bladder. The anterior 
abdominal wall from the umbilicus to the symphysis, the symphysis, 
and the anterior wall of the bladder are absent ; the gap is filled with 
a membrane which represents the posterior wall of the bladder. On 
to this membrane open the ileum, ureters, and vagina. (6) The intes- 
tine is perfectly formed, but the rectum opens into a common sinus 
with the ureters and vagina ; or the ureters open into the cleft blad- 
der, and the rectum and external genitals are united ; or the ureters 
open into the rectum, and the latter terminates normally. 

3. Cloacce combined with Abdominal Hernia. — There is a her- 
nial sac containing all the abdominal viscera. At the lower end of 
the sac is an opening leading into a sinus in which open the lower 
end of the ileum, the bladder or urethra, and the ureters. The rec- 
tum is absent. 

Atresia Ani consists in a deficient development of the colon or 
rectum. The entire colon may be absent ; the rectum may be absent, 
or represented by a solid cord ; or the upper or lower part of the 
colon may be absent, or separated by a solid cord. 

More rarely blind terminations of the small intestines are found, 
and sometimes a narrowing so complete as to close the canal. 

The intestines are also found abnormally shortened in various de- 
grees. A colon of unusually large size has been described as of 
occasional occurrence. * 

INCARCERATION. 

1. The most common form is that in which a portion of intestine 
is strangulated by a fibrous band. Such fibrous bands are produced 
by peritonitis or are remains of foetal growth. They pass from the 
intestines to the abdominal wall, or from one part of the intestines to 
another. The intestine becomes in some way caught under one of 
these bands and is compressed by it. The stricture thus produced 
may cause a gradual accumulation of faeces in the intestine above it, 
and may last for a long time before death ensues. In other cases the 
stricture interferes at once with the circulation of the blood ; the in- 
testine is intensely congested, becomes gangrenous, and death takes 
place with the symptoms of general peritonitis. 

2. A portion of intestine becomes caught in some abnormal open- 

^ Formad, University Medical Magazine, June, 1892. 



THE ALIMENTARY CANAL. 465 

ing in the mesentery or omentum, or in the foramen of Winslow, or 
between the two layers of the mesentery. We have seen a case in 
which twelve feet of intestine had passed through a small opening in 
the mesentery. 

3. A coil of intestine makes half a turn at its base, so that the 
two sides of the loops cross at its base. In this way the lumen of 
the intestine is completely closed and the vessels are compressed, so 
that congestion, peritonitis, and gangrene result. This form of in- 
carceration is most frequent in the ascending colon. In the small 
intestine it only occurs when the gut is fixed by old adhesions. 

4. A portion of the intestine, with its. mesentery, makes one or 
more complete turns on itself, closing the canal and compressing the 
vessels. 

5. A portion of the intestine makes a half or entire turn about its 
longer axis. This is very rare, and only occurs in the colon. 

6. The mesentery of a part of the intestine is long and loose, in 
consequence of a dragging down of the intestine by a hernia or by 
habitual constipation. The portion of intestine thus permitted to 
hang down is habitually filled with faeces, and by its pressure on 
some other part of the intestine produces an incomplete stricture. 

INTUSSUSCEPTION. 

This change of position consists in the invagination of one por- 
tion of intestine in another portion. Usually this takes place in the 
direction of the peristaltic movements, from above downward ; more 
rarely in the opposite direction. 

The parts are found in the following condition : There are three 
portions of intestine, one w^ithin the other. The inner portion is 
continuous with the intestines above the intussusception ; its peritoneal 
coat faces outward. The outer portion is continuous with the intes- 
tine below ; its peritoneal coat also faces outward. The inner portion 
is turned inside out, its mucous membrane is in contact w^th the 
mucous membrane of the outer portion. In rare cases the intus- 
susception is complicated by the invagination of a second portion of 
intestine in the inner tube, and even by a third intussusception into 
the second one. These changes occur both in the large and small 
intestine ; most frequently the lower part of the ileum is invagi- 
nated in the colon. The invaginated portion may be from a few 
inches to several feet in length. The lesion is most frequently found 
in early childhood. 

The intussusception. In' the dragging and folding of the nioson- 
tery which it produces, causes an intense congestion of the parts, and 
even large luBmorrhages between the coats of the intestine. The 
congestion may induce fatal peritonitis, or gangriMie of the intestine. 



466 THE ALIMENTARY CANAL. 

or chronic inflammation and adhesions, and the patient lives for a 
considerable time with symptoms of stricture. In other cases the 
invaginated portion of intestine sloughs, the outer and inner portions 
become adherent, and the patient recovers, with or without some de- 
gree of stricture. 

Besides this grave form of intussusception we often find, es- 
pecially in children, one or more small invaginations not attended 
with congestion or inflammation. These are formed during the death 
agony or immediately after death. 

TRANSPOSITION. 

The position of the intestines may be the opposite to that which 
is usually found. The transposition may affect all the abdominal 
viscera, or only a single viscus is transposed. 

WOUNDS — RUPTURES. 

Penetrating wounds of the intestine usually prove rapidly fatal, 
either from shock or from peritonitis. Sometimes, however, the 
wound becomes closed by the formation of adhesions with the 
neighboring parts. Sometimes the wound in the intestines becomes 
adherent at the position of the wound in the abdominal wall, and an 
intestinal fistula is formed. 

Rupture of the small intestine is not infrequently produced by se- 
vere blows on the anterior abdominal wall. It is noticeable that such 
blows may not produce any marks or ecchymoses of the skin. Such 
ruptures usually prove fatal very soon, but sometimes the patient 
lives several days and the edges of the rupture undergo inflamma- 
tory changes. 

Strictures of the intestine are sometimes followed by rupture of 
the dilated intestine at some point above the stricture. 

THE SMALL INTESTINE. 
INFLAMMATION. 

Acute Catarrhal Inflammation of the greater part of the small 
intestine is developed as part of the lesion of cholera morbus, and 
after the ingestion of irritant poisons. 

Acute inflammation of the duodenum accompanies gastritis, and 
occurs as an idiopathic condition. 

Acute inflammation of the ileum occurs as an idiopathic condi- 
tion, and accompanies inflammation of the colon and of the solitary 
and agminated lymph nodules. 



THE ALIMENTARY CANAL. 4G7 

In many of these cases we infer the existence of the inflamma- 
tion from the chnical symptoms. 

After death the most marked lesions are the increased produc- 
tion of mucus and the congestion. In very severe cases the inflam- 
mation may extend to the peritoneal coat. 

Chronic Catarrhal Inflammation of the small intestine accom- 
panies heart disease, phthisis, emphysema, cirrhosis of the liver, and 
Bright's disease. The intestine is coated with an increased amount 
of mucus ; it is often congested ; there may be a general thickening 
of all its coats. 

Croupous Inflammation is produced by irritant poisons; it is 
associated with croupous colitis, and it occurs as an idiopathic disease. 
The mucous membrane is coated with fibrin, its stroma is infiltrated 
with fibrin and pus, and this infiltration extends to the connective 
tissue, muscular and peritoneal coats. 

Suppurative Inflammation of the submucous connective-tissue 
coat is said to occur in rare cases. It is usually metastatic. It takes 
the form of purulent foci of variable extent, which perforate either 
inward or outward. 

THE SOLITARY AND AGMINATED GLANDS (lYMPH NODULES). 

It is not uncommon to find in healthy adults who have died from 
accidental causes a considerable swelling of the solitary and agmi- 
nated glands (lymph nodules) of the ileum, without any reason 
which we can discover to account for this swelling. 

Extensive burns of the skin may be followed by a very marked 
swelling of the solitary and agminated nodules. 

In persons who have died from the infectious diseases it is not 
uncommon to find these nodules swollen. 

In children, swelling of these nodules, often followed by softening 
and the formation of ulcers, accompanies many of the catarrhal in- 
flammations of the large and small intestines. 

In pulmonary phthisis we ver}^ frequently find changes in the 
solitary and agminated nodules of the small intestine, less frequently 
in the solitary nodules of the colon. The changes seem to be of the 
same character as those which take place in tubercular inflammation 
of lymphatic nodules in other parts of the body. 

The nodules become swollen, their elements are multiplied, tuber- 
cle granula are formed, the central portions of the nodules become 
cheesy. The cheesy degeneration extends ; it is followed by soften- 
ing and by death of the mucotis membrane over the nodules : the 
softened tisstie is discharged into the intestine, ami ulcers are formed 
with overhanging edges. After this the tilcer slunvs no teiulency to 
heal, but, on tlie contrary, beconu^s la,ri2:er. usuallv exteiulinu* late- 



468 THE ALI.AIEXTAEY CAXAL. 

rally so as sometinies to nearly encircle the gut. After death we 
find, in different patients, these ulcers in all their stages of develop- 
ment. They vary much as to the proportion betTreen the tubercular 
and the ordinary inflammatory changes. In some the tubercle 
granula are nmnerous, in others they are few or even absent alto- 
2'ether. The tubercle bacilh are verv constantlv found in them. 
There is also usually a tubercular inflammation of the peritoneum 
over the ulcers, and sometimes of the lymphatics and nodes of the 
mesentery. Although these ulcers often reach a large size, it is but 
very seldom that they perforate into the peritoneal ca^dty. 

Ulcers of the Duodenum. — A few cases have been recorded in 
which extensive burns of the skin have been followed within a few 
days by the formation of deep ulcers of the duodenum. It is still 
uncertain how these ulcers are produced. 

Chronic perforating ulcers, resembling the chronic ulcers of the 
stomach, are found in the duodenum. They are associated with 
similar ulcers in the stomach or occur by themselves. 

Some curious ulcers of the upper part of the small intestines are 
described by Israel. ^ There were five ulcers, from two and one-half 
to ten centimetres long, encircling the intestine, with irregular, 
granulating surfaces. 

SypliiUtic ulcers produced by changes in the solitary and agmi- 
nated glands of the small intestine are sometimes found in infants. 

EMBOLI. 

Emboli have been found in the superior mesenteric artery in a 
niunber of cases ; in the inferior mesenteric artery they are less fre- 
quent. They produce an intense venous congestion of the entire 
wall of the intestine, "with haemorrhage into its cavity and its wall. 

THE LARGE IXTESTIXE. 

IXFLAMMATIOX. 

The mucous membrane of the large intestine is very frequently 
the seat of acute and chronic inflammatory processes. The larger 
number of these belong to the condition which is described chnicaUy 
under the name of dysentery. The inflammation affects most fre- 
quently the recttim, sometimes the entire length of the colon, some- 
times only the upper part of the colon. 

Acute Catcirrlial Colitis. — The lower end of the colon is the 
portion most frequently involved in this form of inflammation, but 
it may be its upper end or the entire length of the gut. The name 

^ Charite-Annalen, 18S4, p. 707. 



THE ALIMENTAKY CANAL. 469 

catarrhal colitis is the only term used at the present time to desig- 




FiG. 229.— Catarrhal Colitis. 
Showing swollen lymph nodule. 



nate four morbid conditions of the colon, which differ from each 
other both in their anatomical and clinical features. 






■4 , 




Fig. 230.— Catarrhal CoLrns, productive and necrotic. 

1. The inflammation is of simple exudative typo. It is usually 



470 



THE ALIMEXTAKY CANAL. 



confined to the lower end of the colon, runs its course within a 
week, and is not fatal. The glandular and connective-tissue coats 
of the colon are swollen and congested, with more or less infiltration 
mth serum and pus cells. There is an increased production of mu- 
cus, which coats the surface of the colon and comes away with the 
stools. There may be bleeding from the surface of the inflamed 
mucous membrane. 





/ 



Fig. 231.— CATARRHAii Colitis, productive and necrotic. 

2. The inflammation is. of exudative type, but with an excessive 
production of pus cells. It may involve any part of, or the entire 
length of, the colon. It may cause death within a few days or con- 
tinue for several weeks. The wall of the colon is SAvollen and con- 
gested. The stroma between the tubules, the connective-tissue coat, 
and sometimes the muscular and peritoneal coat, are infiltrated with 
large numbers of pus cells. The solitary nodules may be swollen 
(Fig. 229). There is an increased production of mucus. 



THE ALIMENTARY CANAL. 471 

3. The inflammation is of the productive type with exudation. 
It may involve any part, or the entire length, of the colon. It may 
cause death within a few days, or continue for several weeks, or be 
followed by a chronic colitis. The wall of the colon is swollen and 
congested. There is an increased production of mucus. There is a 
large exudation of serum from the blood vessels, which is discharged 
from the bowels in the form of a thin, brownish fluid. There is a 
growth of new connective tissue with an excess of cells, confined to 
the stroma between the tubules or also involving the connective- 
tissue coat. There may also be a considerable infiltration with pus 
cells and swelling of the solitary nodules. 

4. In a colitis of either the purulent or productive type there may 
also be necrosis of the inflamed tissue (Figs. 230 and 231). The ne- 
crosis shows itself by the change of the inflamed tissues into amor- 
phous granular matter, which afterward disappears and leaves losses 
of substance. The necrosis begins on the free surface of the mucous 
membrane and then extends more deeply into it, but not beyond the 
connective-tissue coat. In this way are formed little erosions, so 
small that they cannot be seen with the naked eye, or larger and 
deeper ulcers, or considerable areas of the intestine are entirely de- 
nuded of their glandular coat. In the solitary nodules only the 
centres may be necrotic, or the entire nodule may slough away. In 
this way rounded ulcers with overhanging edges are formed. In 
some cases ulcers are formed partly by necrosis of the glandular 
coat, partly by the destruction of the solitary nodules. 

Ci^oupous Colitis. — This form of inflammation may involve the 
rectum alone, or the entire length of the colon, or only its upper por- 
tion. The mucous membrane is congested and swollen, and coated 
with a layer of false membrane ; the connective tissue between and 
beneath the glandular tubules is infiltrated with fibrin and pus, and 
in severe cases the inflammation involves the muscular and peri- 
toneal coats also. The inflammation is usually more intense at some 
13laces than at others, so that the surface of the mucous membrane 
shows the false membrane in isolated patches (Fig. 232). Less fre- 
quently there is a uniform coating with the false membrane. In mild 
cases, as the inflammation subsides, the products of inflammation are 
absorbed and the wall of the intestine returns to its normal condition. 
In more severe cases the quantity of the inflammator}^ products is so 
great that portions of the wall of the intestine become necrotic. This 
necrosis may involve only the glandular coat, or it may extend deeper 
into the wall of the intestine. Tiie necrosed tissue after a time sloughs 
awaj^ leaving behind ulcers of different sizes and depths. After this 
the ulcers may cicatrize, or their floors and walls may remain in the 
condition of granulation tissue for an indefinite lenLvth of time. When 



472 



THE ALIMENTARY CAXAL. 



the latter is the case there is added a chronic inflammation of the wall 
of the intestine between the ulcers, with changes in the mucous mem- 
brane and thickening of the connective tissue and muscular coats. 

Follicular Colitis (I^odular Cohtis). — In many cases of catar- 
rhal and croupous inflammation of the colon the solitary follicles 
(lymph nodules) become more or less swollen and necrotic. Besides 
these cases, however, there are others in which the changes in the 




Fig. 232.— Croupous Colitis. False membrane in patches. 



nodules form the principal part of the lesion, while the catarrhal or 
croupous inflammation is but slightly developed. The nodules are 
first swollen, then necrotic, then slough away and leave little circular 
ulcers with overhanging edges (Fig. 233). These ulcers are usually 
numerous and extend over a large part of the colon. The patients 
have diarrhoeal rather than dysenteric passages. The ulcers are apt 
to show but little disposition to heal, and the acute colitis often becomes 



THE ALIMENTARY CANAL. 



473 



chronic. It seems probable that some of the cases which look like 
follicular colitis are really exaraples of amoebic colitis. 

Amcebic Colitis. — This form of colitis is caused by the presence 
in the wall of the intestine of amoebae. These organisms were first 
recognized by Lambl in 1859. Since then they have been described 
by a number of observers, most fully by Kartulis and by Councilman 
(seepage 103). 



■-.:...-^.-^/-;i;;^><''^^'"'^'r:T-*??''^'-"''-^.r.,„^,, 



.X 



■^ 




Fig, 233— Follicular (^Nodular) Colitis. 



The amoebae are found in the little, gelatinous masses which are 
found in the stools. They are of rounded shape, and, whon alivo, 
change their position and shoot out and retract little projections 
(pseudopodia). Their outer portion is composed of a pale liyalin 
or homogeneous substance ; the inner contains vacuoles and is more 
refractive. 

In the colon the amcebiB are found in the connective-tissue coat 
and in the floors of the ulcers. Tlie principal eiVect of tlie presence 
41 



474 THE ALI3IEXTARY CAXAL. 

of the amoebae seems to be the death of the tissues in which they are 
lodged, with more or less swelling and infiltration of the surrounding 
parts. In this way are formed httle, round ulcers which resemble 
f ohicular ulcers • larger and deeper ulcers ; or extensive sloughs of 
considerable portions of the mucous membrane. 

In some, cases of amoebic cohtis the organisms are found also in 
the hver and produce in it the same necrotic changes. 

Chronic Colitis. — If a chronic inflammation of the colon has 
continued for any length of time, the wall of the gut is found to be 
very much changed. The glandular coat may be imiformly thick- 
ened, or throTTQ into the form of polypoid tiunors. or atrophied, or de- 
stroyed by ulcers of various sizes and shapes. The connective-tissue 
and muscular coats may be thickened or thinned. Apparently 
chronic cohtis may follow any of the forms of acute cohtis. 

Tlie Ccecum. — Catarrhal inflammation of the caecum is not un- 
common. It is usually produced by an habitual accumulation of fae- 
ces in this part of the intestine. The course of the infl.ammation is 
chronic, but marked by acute exacerbations. At fii'st the mucous 
membrane imdergoes the ordinary changes of chronic catarrhal in- 
flammation : then there is a slow suppurative inflammation vrhich 
extends through the wall of the intestine and produces ulcers and 
perforations. Thi'ough these perforations the faeces may pass into 
the peritoneal cavity, or the jDerf orations are partly closed by adhe- 
sions, and abscesses are formed, or sinuses into the surrounding soft 
parts. 

Tlie Bectum. — Besides the inflammatory changes already de- 
scribed as existing in the colon, we sometimes find a suppurative in- 
flammation of the connective tissue which surrounds the rectum, 
either associated with lesions of the mucous membrane or occur- 
ring by itseK. 

In adults the lower end of the rectum is the part of the intestine 
which is the most frequent seat of syphilitic ulceration. ^lost of 
these tilcers seem to be the result of imnatural coitus, or of infection 
from specific sores of the vulva ; but some of them seem to be due 
to the softening of gummy tumors. 

The Vermiform Appendix. — The appendix is given ofl^ from the 
inner and posterior asj^ect of the lower end of the caput coh. It is 
from three to six inches in length. It may be turned upward be- 
hind the caecum, or it may hang downward free in the peritoneal 
cavity. It is composed of peritoneal, muscular, connective-tissue, and 
glandular coats. 

1. The mucous membrane may be the seat of acute catarrhal in- 
flaromation. This is of mild tyi^e and short duration, with conges- 
tion, swelling, and an increased production of mucus ; or it is of 



THE ALIMENTARY CANAL. 475 

severer type, of longer duration, and the cavity of the apj^endix is 
distended by large quantities of mucus and pus. 

2. The entire thickness of the wall of the intestine may be the 
seat of an acute exudative inflammation. The appendix is very 
much increased in size, sometimes to the size of a man's finger. This 
increase in size is due, not to a dilatation of the cavity of the appen- 
dix, but to a thickening of its walls. The walls are congested, swol- 
len, infiltrated with fibrin and pus, the peritoneal coat covered with 
fibrin. There is no necrosis and no perforation. If the appendix is 
behind the caecum, or if adhesions are formed early, there is only a 
localized peritonitis. If the appendix projects freely into the peri- 
toneal cavity and no adhesions are formed, a general peritonitis is 
soon established. 

3. At one or more points in the wall of the appendix there is an 
exudative inflammation with necrosis. In this way small or large 
portions of the wall of the appendix are destroyed, large or small 
perforations are formed, and the contents of the appendix escape 
into the abdominal cavity. In these cases the appendix usually 
contains a fsecal concretion. Such perforations are regularly fol- 
lowed by the formation of an abscess around the appendix. The 
pus may extend from this abscess in any direction and for long dis- 
tances, so that we find abscesses deep in the pelvic cavity, or under 
the diaphragm J or at other remote points. 

4. The entire appendix becomes gangrenous within one or two 
days, with the formation of an abscess, or general peritonitis. This 
is the most fatal form of appendicitis ; its pathology is obscure. 

5. In catarrhal or croupous colitis the inflammation may extend 
to the appendix. 

6. In typhoid fever there may be changes in the wall of the ap- 
pendix of the same character as those in the wall of the small intes- 
tine. 

7. There may be a tubercular inflammation of the appendix, ^Wtli 
the formation of ulcers. 

TUMORS. 

Myomata. — Tumors composed of smooth muscle and connective 
tissue grow in the muscular coat and project inward. They may be 
large enough to obstruct the intestine, and may then give rise to 
intussusception. In the duodenum such tumors may obstruct tho 
common bile duct. Less frequently these tumors project outward 
into the peritoneal cavity. 

Lipomata may be developed from the submucous coat and grow 
inward, or from the subserous coat and project outward into tho 
peritoneal cavity. 



470 THE ALIMENTARY CANAL. 

Polypoid Tumors, projecting into the cavity of the intestine and 
composed of connective tissue and covered with epithelium, are fre- 
quently found. They are associated with catarrhal inflammation or 
occur by themselves. They are found throughout the intestinal 
tract and may be single or multiple. They grow from the submucous 
coat and project inward. Some of them are small, solid, connective- 
tissue tumors, covered by the mucous membrane which they have 
pushed inward. Others are of the same character, but of large size. 
In others the connective tissue is arranged in branching tufts, covered 
with cylindrical epithelium; and in these last tumors there may also 
be tubules lined with cylindrical epithelium, giving to the growth 
the characters of an adenoma. 

Adenomata are found in the duodenum and colon. They form 
flat infiltrations of the wall of the intestine, or project inward as poly- 
23oid tumors. They are composed of tubular follicles, like those of 
the intestinal mucous membrane, and of a connective-tissue stroma. 
In some of these tumors the tubules have a tolerably regular shape 
and arrangement ; there is no infiltration of surrounding tissue ; the 
tumor is of benign nature. In other tumors the tubules are irregular 
in shape and arrangement, and the growth infiltrates the surround- 
ing parts. There is no sharp dividing line between these tumors and 
the carcinomata. 

Carcinomata are found in the colon and the duodenum, and are 
of three varieties. 

1. The new growth is composed of tubules hned with cylindrical 
epithelium. It begins as a flat infiltration of the submucous coat, 
which soon surrounds the intestine, infiltrates the whole thickness of 
the wall of the gut, and may extend to the surrounding soft parts. 
Fungous masses project into the cavity of the intestine, while at the 
same time ulcerative and destructive processes are going on. Ac- 
cording to the exact arrangement of the growth, there is more or less 
stenosis of the intestine. 

2. The growth has the characters of colloid cancer and forms a 
diffuse infiltration of the intestinal wall, completely surrounding it 
and often extending over a length of several inches. 

3. At the anus there is sometimes a carcinomatoiis growth, with 
flat epithelial cells (epithelioma), like similar growths in the skin, 
which involves the lower end of the rectum. 

Lymphoma. — Tumors composed of tissue resembling that of the 
lymphatic glands originate in the solitary and agminated nodules, 
and in the intestinal wall in cases of leukaemia and pseudo-leukcemia. 

Similar tumors are found as an idiopathic lesion both in the large 
and small intestines. These tumors are irregular, diffuse growths 
infiltrating the wall of the intestine, the mesentery, and the neigh- 



THE ALIMENTARY CANAL. 47? 

boring lymph nodules, and reaching a considerable size. They often 
ulcerate internally and produce dilatation or stenosis of the intestine. 
It is hard to tell whether some • of these tumors should he caUed 
lymphomata or sarcomata. 

CONCRETIONS, 

There are sometimes found in the intestines round, oval, or irreg- 
ular masses of firm consistence. They are usually small, but may 
reach the size of a man's fist. They are composed of fsecal matter, 
mucus, bile, the carbonate and phosphate of hme, and triple phos- 
phate. They may produce inflammation, ulceration, and perforation. 

PARASITES. 

Mycosis intestinalis. — Under this name have been described a 
number of cases in which inflammation of the intestines occurred as 
one of a group of lesions. ^ In these cases there are found ecchymoses 
of the skin and mucous membranes ; patches of fibrin in the stomach, 
small intestine, and colon ; serum in the peritoneal cavity ; swelling 
of the spleen and lymphatic glands ; and sometimes inflammation of 
the lungs. The intestinal lesions are most marked in the small in- 
testine and the upper part of the colon. The mucous membrane is 
studded with small brownish patches. At the centres of these 
patches the wall of the intestine is infiltrated with pus, and around 
the centres it is infiltrated with blood. Bacilli resembling those of 
anthrax are found in the intestinal lesions and in other parts of the 
body. It is believed that the disease is a form of anthrax. 

Ascaris lumhricoides is found in the small intestine, either singly 
or in considerable numbers. In rare cases a number of worms may 
form a mass which produces infiammation, ulceration, and perfora- 
tion. 

Oxyui'is vermicularis is found in large numbers in the rectum. 

Tricocephalus dispar is found in the caecum. 

Ankylostonium duodenale is found in the duodenum and may 
give rise to considerable haemorrhages. 

Trichina spiralis is found in its adult condition in the small in- 
testine. 

Pentastomuni denticulatiini occurs in the submucous tissue of 
the small intestine in an encapsulated condition. 

Cysticercits cellulosoi has been seen, in a few cases, on the mu- 
cous membrane. 

^ Vircli. Arch., Bd. xxi., p. 579 ; xxx., p. 300 ; lii.. p. 541. Zeitsch. fi\r Biologic, 
T., p. 129. Arch, der Heilkunde, xv. Arch. fUr klin. :Med.. xii.. p. 517. 



478 THE ALIMENTARY CANAL. 

Tcenia solium, Taenia mediocanellata, and Botliriocephalus 
latus are all found in the small intestine. 

Yeiy large numbers of various forms of bacteria are regularly 
found in the intestinal cavity, intermingled with its contents and 
clinging to its walls. Among the most common of these is the 
Bacillus coli communis (see page 205). 

THE PERITONEUM. 

The free surface of the parietal peritoneum is covered with a single 
layer of flat, polygonal, nucleated cells. Beneath these cells are succes- 
sive planes of connective tissue extending down to the muscles and 
fasciae. These planes are formed of a fibrillated basement substance 
reinforced by elastic fibres, and of branching cells. Embedded in the 
connective tissue are the nerves, blood vessels, and lymphatics. The 
lymphatic system is very extensive. 

The omentum consists of fibrillated connective tissue arranged so 
as to form a meshwork. The trabeculse of the meshAvork are com- 
pletely covered by large, flat cells. In the basement substance, be- 
neath the endothelium, are branching cells. In the larger trabeculse 
are blood vessels, lymphatics, and fat. Sometimes we find on the 
larger trabeculse little nodules formed of polygonal or branched cells. 

MALFORMATIONS. 

Arrest of development of the peritoneum occurs in the shape of 
fissures in the mesial line or external to it ; in the case of the dia- 
phragm being absent, of a fusion with the pleura ; and as defective 
development of the mesentery, the omentum, and the other folds of 
the peritoneum. 

Excess of development occurs in the shape of unusual length of 
the mesentery, the omentum, and the other folds of the peritoneum ; 
or of supernumerary folds and pouches. These are chiefly found in 
the hypogastric, iliac, and inguinal regions and near the fundus of 
the bladder. There is access to these sacs by a well-defined fissure or 
ring, which is frequently surrounded by a tendinous band lying in 
the duplicature. They may give rise to internal incarceration of the 
intestines. 

INFLAMMATION. 

The very great extent of the peritoneum, and the readiness with 
which its lymphatic system absorbs foreign matters from the perito- 
neal cavity, render peritonitis a most severe and dangerous form of 
inflammation. 

If the greater part of the peritoneum is inflamed we call the lesion 
a general peritonitis. If only a circumscribed area is involved it is 



.THE ALIMENTARY CANAL. 479 

^ local peritonitis. The course of the inflammation may be rapid or 
slow, so that we speak of acute and chronic inflammation. The 
inflammation may be attended with the production of tubercle tissue, 
and then it is a tubercular peritonitis. 

I. Acute Peritonitis. 

The acute inflammations of the peritoneum may occur as idio- 
pathic lesions without discoverable cause ; but much more frequently 
they are directly due to some appreciable cause. 

Wounds and contusions of the wall of the abdomen ; wounds, ulcers, 
new growths, incarcerations, intussusceptions, ruptures, perforations, 
and inflammations of the stomach and intestines ; inflammation of the 
vermiform appendix ; injuries, ruptures, and inflammations of the 
uterus, ovaries, and Fallopian tubes ; rupture and inflammation of 
the bladder ; inflammation of and about the kidneys ; abscesses and 
hydatid cysts of the liver ; inflammation of the gall bladder and 
large bile ducts ; thrombosis of the portal vein ; inflammations of the 
spJeen, pancreas, lymphatic glands, retroperitoneal connective tissue, 
vertebrse, ribs, and pelvic bones ; septicsemia and the infectious dis- 
eases, and chronic Bright^s disease — are all ordinary causes of acute 
peritonitis. 

According to the exact cause of the inflammation, the peritonitis 
is at first either local or general. A local peritonitis may remain cir- 
cumscribed, or it may spread and become general. 

We can distinguish two anatomical forms of acute peritonitis. 

1. Cellular Peritonitis. — This form of peritonitis may be pro- 
duced by any irritant which does not act too energetically. It can be 
excited in dogs by injections of very small quantities of a solution of 
chloride of zinc. In the human subject we find it with perityphlitis, 
with circumscribed abscesses in the peritoneal cavity, and in cases 
of puerperal fever which die within forty-eight hours after the devel- 
opment of symptoms. 

After death Ave find the entire peritoneum of a brigl it-red color 
from the congestion of the blood vessels ; but there are no fibrin, no 
gcrum, no pus, no other lesions visible to the naked eye. ^linute 
exannnation, however, shows a very marked change in the endo- 
thelial cells. They are increased in size and number, and the new 
cells coat the surface of the peritoneum and project outward in little 
masses (Fig. 234). 

2. Exudative Peritonitis. — The ordinarv form of acute iHMitt^- 
nitis is attended with the production of serum, fibrin, and pus. and 
with changes in the endothelium and connective-tissue cells. 

If we inject a solution of chUn-ide of zinc or of some other irri- 
tant into the peritoneal cavity of a dog, we find that by tlie end of 



480 



THE ALIMENTARY CANAL. 



one or two hours infianiniatory changes are e\adent. There is a lit- 
tle serum in the peritoneal cavity, a general congestion of the peri- 
toneum, and little knobs and threads of fibrin on its surface. There 
are no marked changes in the endothelium or connective- tissue cells, 
but pus cells are present, in moderate numbers in the stroma just be- 
neath the endothelium, and white blood cells in the vessels. 

After the lapse of twenty-four hours the lesions are more marked. 
The congestion of the peritoneum is much more decided, there is 
more serum in its cavity and a thicker layer of fibrin and pus on its 










Fig. 234.— Acute Ceixular Peritonitis. 
Human omentum, X 750 and reduced. 

surface. Minute examination shows that two distinct sets of chan- 
ges are going on at the same time : (1) a production of fibrin, se- 
rum, and pus ; (2) a swelling and multiplication of the endothelial 
cells. If the inflammation is very intense the pus and fibrin are 
most abundant ; if the inflammation is milder the changes in the 
endothelium are more marked. The fibrin coagulates on the free 
surface of the peritoneum. The white blood cells collect in large 
numbers in the blood vessels, and as pus cells infiltrate the stroma 
and collect on its surface. There is no special change in the con- 
nective-tissue cells. The endothelial cells may remain in place. 



THE ALIMENTARY CANAL. 



481 



although their edges and corners are separated by pus cells and knobs 
of fibrin ; or the endothelium falls off in large patches ; or the sur- 
face of the peritoneum is covered with numerous cells which look 
like endothelial cells more or less deformed. But few dogs survive 
the third day of an acute artificial peritonitis. 

In the human subject, if death takes place before the third day, 
both the gross and minute changes are the same as those seen in 
the dog. There are present the same general congestion, the pus, 
fibrin, and serum, the desquamation and multiplication of the endo- 
thehal cells (Fig. 235). 










FiG. S35.— Acute Exudative Peritonitis, eight days' ouration. 
Human omentum, x 850 and reduced. 

In many cases of peritonitis, however, death occurs between the 
«ixth and fourteenth days of the disease. The appearance of the 
peritoneum at this period of the infiammation is not always the 
same. The congestion of the blood vessels may persist, it may be 
very intense and accompanied with extravasations of blood, or it 
may be entirelv absent. There mav be a thin coatini>' of fibrin and 
pus gluing together neighboring surfaces of peritoneum, or this layer 
may be very thick. The accumulation of pus may be superficial, or 
it may infiltrate the whole thickness of the peritoneum and the sub- 
peritoneal connective tissue. The quantity of purulent serum in the 
peritoneal cavity may be small or large, and tiiis serum may contain 



482 



THE ALIMENTARY CANAL. 



few or many pus cells, or the serum may be of a dirty -brown color 
and filled with bacteria. When the purulent serum is shut in by 
adhesion it is often thick and yellow, like the pus of an abscess. 

The minute appearances differ from those seen at an earlier stage, 
chiefly in the larger amount of inflammatory products and in the 
changes in the fixed connective-tissue cells. During the first three 
days of an acute peritonitis the connective- tissue cells are but little 
changed, but by the seventh day there is a marked increase in their 
size and number. 

Acute peritonitis may prove fatal by the fourteenth day ; or it 
may be succeeded by chronic peritonitis ; or the patients recover and 






I 












^ ^ 







/ 







/^^ 



Fig. 236.— Chronic Cku^tilar Peritonitis occurring with Pulmonary Phthisis. 
Human omentum, x 750 and reduced. 

permanent connective-tissue adhesions and thickenings of the peri- 
toneum are left behind. Recovery is most common when the peri- 
tonitis has been a local one. 



11. Chronic Peritonitis, 

We find the following varieties of chronic peritonitis : 
1. Cellular Peritonitis. — This form of peritonitis is found as a 
complication of chronic endocarditis, of cirrhosis of the liver, of 
chronic pulmonary phthisis, and of acute general tuberculosis. 

Neither fibrin nor pus is present, but there may be clear serum in 



THE ALIMENTARY CANAL. 483 

the peritoneal cavity. The peritoneum may look normal to the naked 
eye, or it may be studded with very minute, translucent nodules. 

Minute examination shows changes in the endothelial cells and 
the connective-tissue cells. These cells are everywhere increased in 
number and altered in shape ; or, to speak more guardedly, the sur- 
face of the peritoneum is covered with cells which look as if they 
were derived from the endothelium and the connective- tissue cells 
(Fig. 236). Some are large, flat cells ; some smaller, polygonal 
cells ; some irregularly fusiform ; some large, granular masses con- 
taining a numher of nuclei. Although these new cells are found 
over most of the surface of the j^eritoneum, yet they are more nu- 
merous in little patches which are scattered here and there. 

2. Peritonitis with Adhesions. — There may be a formation of 
permanent adhesions without the production of fibrin or pus. It is 
often, indeed, difficult to tell whether old peritoneal adhesions are due 
to the form of chronic peritonitis of which we are now speaking, or 
whether they are the result of an acute peritonitis. But there are 
some cases in which the mode of development of the adhesions seems 
evident. 

If, from perityphlitis or some other cause, a collection of pus is 
shut in in some part of the peritoneal cavity, we may find the rest of 
the peritoneum smooth and shining ; no serum, fibrin, or pus, no 
thickening ; but the neighboring surfaces of the peritoneum are at- 
tached to each other by adhesions. These adhesions are in the shape 
of threads and membranes, often of the most extreme tenuity. They 
are f orixied of a fibrillated basement substance, the fibrils crossing 
each other in all directions. In the basement substance are cells, 
some fusiform and stellate, but most of them look like large branch- 
ing cells, of which the cell bodies have become fused with the base- 
ment substance while the nuclei remain. 

Close to these adhesions the peritoneum may appear normal to the 
naked eye, but if it is put in water very fine threads and membranes 
will float upward from its free surface. Minute examination shows 
that the connective-tissue cells are increased in size and number, that 
the endothelial cells are replaced by cells of a great variety of shapes, 
and that the thin little threads and membranes on the surface are 
formed of large branching cells (Fig. 237). 

Such a peritonitis with adhesions appears to be a more advanced 
stage of the cellular peritonitis just described, but the infianunation, 
instead of stopping at the production of cells alone, goes on to the 
formation of membranes. 

We sometimes find in the same patient chronic pleurisy with adlu^- 
sions and chronic peritonitis with adhesions. 

3. Chronic ]\>rifon His (('if h Thii'k-c((ii((j of f/ic PcrifoKCioK. — 



484 



THE ALIMENTARY CANAL. 



This form of peritonitis occurs quite frequently as an idiopathic 
lesion. It may involve the greater part of the peritoneum or be con- 
fined to the capsules of the liver and spleen. 

The most marked feature of the lesion is the thickening of the peri- 
toneum — a thickening which may reach as much as an inch. The 
outer portions of the thickened peritoneum are composed of dense 
connective tissue, the inner layers of granulation tissue. The surface 
of the peritoneum is smooth or covered with fibrin. There may also 
be connective-tissue adhesions between different parts of the perito- 
neum. The peritoneal cavity contains clear or purulent serum. 







Fig. 237.— Chronic Peritonitis with Adhesions, x 750 and reduced. 

Parietal peritoneum. 

In some cases the parietal peritoneum is principally involved ; in 
others the peritoneum of the stomach, intestines, liver, and spleen. 
The thickening of the capsule of the liver is attended with a diminu- 
tion in the size of that viscus. 

4. Chronic Peritonitis with the Production of Fibrin, Serum, 
and Pus. — This form of peritonitis may follow acute peritonitis, may 
be due to lesions of the abdominal viscera, or may occur without 
known cause. 

The abdominal cavity contains purulent serum, either free or shut 



THE ALIMENTARY CANAL. 485 

in by adhesions. The surface of the peritoneum is coated with fibrin 
and connective-tissue adhesions. The coils of intestine, and all the 
neighboring surfaces of the peritoneum, are matted together partly 
by fibrin, partly by permanent adhesions. 

5. Hcemorrhagic Peritonitis. — This occurs most frequently as a 
local inflammation. It involves the peritoneum behind and around 
the uterus in the female, and that covering the recto-vesical excava- 
tion in the male. The affected portion of the peritoneum is covered 
with layers of new membrane infiltrated with blood. The membranes 
are formed of connective tissue containing numerous blood vessels 
and infiltrated with blood. The extravasations of blood may form 
tumors of considerable size. 

General hsemorrhagic peritonitis is described by Friedreich. ^ In 
two cases of ascites, which had been frequently tapped, he found the 
visceral and parietal peritoneum covered with a continuous mem- 
brane of a diffuse yellowish-brown color, mottled with extravasations 
of blood. The membrane was thickest over the anterior abdominal 
wall. It could be separated into a number of layers. These layers 
were composed of blood vessels, masses of pigment, branching cells, 
and fibrillated basement substance. In many places the extravasated 
blood was coagulated in the shape of round, hard, black nodules. 
The entire new membrane could be readily stripped off from the 
peritoneum. 

6. Tubercular Peritonitis. — This occurs as one of the lesions of 
acute general tuberculosis, with chronic pulmonary phthisis, with 
tubercular inflammation of the genito-urinary tract, and as a local 
inflammation. 

The gross appearance of the lesion varies. 

When tubercular peritonitis occurs as one of the lesions of generrJ 
tuberculosis, there are numerous small miliary tubercles, increase in 
the size and number of the endothelial and connective- tissue cells, and 
sometimes a little fibrin. Some of the miliary tubercles are com- 
posed of tubercle tissue, others of round and polygonal cells. 

As a complication of tuberculosis of the genito-urinary tract ^ve 
find the peritoneum studded with miliary tubercles, coated with fibrin, 
and serum is also present in the peritoneal cavity. 

As a complication of chronic phthisis there are miliary tubercles 
in the peritoneum of the small intestine immediately over the tuber- 
cular ulcers of the mucous membrane. There mav also be thickeniuir 
of the peritoneum and permanent adhesions. 

Local tubercular peritonitis usually follows one of three types : 

(a) Tnhercidar Ascites. — The peritoneum is thickened : it is 

J Virch. Airh.. Pxl. Iviii.. p. 35. 



4S6 THE ALIMENTARY CANAL. 

Studded Tvith masses of tubercle tissue in tlie form of miliarv 
tubercles or of large, flat masses. The omentum may be much 
thickened. There are but few adhesions, but there is a large amount 
of turbid serum. There may be at the same time tubercular pleurisy, 
or tubercles in the spleen or in the h^nphatic glands (lymph nodes). 

(b) Tubercular Peritonitis with the Production of a large 
amount of Fibrin. — The peritoneum is studded with miliary tuber- 
cles. It is coated with a thick layer of soft, gelatinous fibrin, which 
mats together all the neighboring peritoneal surface, so that the 
abdominal cavity seems to be filled with a large, boggy mass com- 
j)osed of all the viscera adherent to each other, and with the inter- 
stices between them fiUed with fibrin. 

(c) Tubercular Peritonitis ivith Adhesions. — The peritoneum 
is thickened and there are numerous connective-tissue adhesions. 
All the abdominal viscera are firmly matted together, and there may 
be collections of pus shut in by the adhesions. The adherent coils 
of intestine may ulcerate and open into each other. There are miliary 
tubercles, or large tubercular nodules or plates. 

TUMORS. 

Fibromata are developed from the subperitoneal connective tissue 
and project inward into the peritoneal cavity. They are found 
beneath the parietal peritoneum and that covering the intestines. 
Such tumors may reach a very considerable size. Papillary fibro- 
mata of the peritoneum may be secondary to papillary fibroma of the 
ovary. 

Lipomata. — Circumscribed tumors composed of fat tissue are 
formed beneath the intestinal and parietal peritoneum and in the 
mesentery. These tumors may become changed into fibrous tissue 
or calcified. Their pedicles may become atrophied so that they are 
left free in the peritoneal caA^ity. 

When they grow beneath the parietal peritoneum they may 
form fat hernise. At the umbilicus, in the inguinal canal, along the 
vas deferens, in the crural ring, and in the foramen obturatorium, 
fatty tumors may grow, project outward under the skin like hernise, 
and, by dra'vving the peritoneum after them into a pouch, may open 
the way for a future intestinal hernia. 

Plexiform Angio-Sarcoma. — Yery large tumors, resembling in 
their gross appearance colloid cancer, have been described by Wal- 
deyer. ^ They are formed by a new growth of blood vessels, with a 
production of gelatinous tissue from their adventitia. 

Carcinoma of the peritoneum is either secondary or primary. 

^ Yirch. Arcli., Bd. Iv., p. 134. 



THE ALIMENTARY CANAL. 487 

The primary tumors assume the character of colloid cancer or of com- 
mon cancer. 

The colloid form frequently involves the greater part of the perito- 
neum, and forms a large mass which distends the abdomen. The 
omentum is changed into a large, gelatinous mass ; the subjacent 
muscles, the lymphatic glands, and the liver are infiltrated with the 
new growth, and soft, gelatinous masses project into the peritoneal 
cavity. The umbilicus is sometimes invaded, so as to project out- 
ward in the form of a semi-translucent tumor. The appearance of the 
new growth is that of a soft, jelly-like mass embedded in a fitjrous 



\ -^ , \ ^ \ v^-"^*""^."^ M / 



-^ ^ ^ 



1 h p J 






\ 






'^'^"t:l&., -"' \ ' 






\ <>■ 

















I "*^J^-'l^ 






J 

1 



Fig. 238.— Section op a Retroperitoneal Sarcoma, x 850 and reduced. 

stroma. The minute structure is that of a connective-tissue stroma, 
arranged so as to form cavities of different sizes. These cavities are 
filled with a homogeneous, gelatinous basement substance and with 
polygonal cells. 

Common carcinoma appears in the form of numerous small nod- 
ules scattered everywhere in the inner layers of the peritoneum. 
These nodules are small, firm, and white, and are composed of a 
fibrous stroma enclosing cavities filled with polygonal cells. With 
the formation of these nodules there are often associated a general 
thickening of the peritoneum, an accumulation of serum in the perito- 
neal cavit}^, and adhesions. 



488 THE ALIMENTARY CANAL. 

Endotlieliomata of the peritoneum have been observed in cases 
with similar growths in the pleura (page 349). 

Sarcomata appear in the form of solitary, slowly growing tumors 
behind the peritoneum or between the folds of the mesentery. 

These retroperitoneal sarcomata are found both in children and 
adults. They usually originate behind the peritoneum covering the 
posterior part of the abdominal wall. At first they grow slowly in- 
Avard, pushing forward the peritoneum and abdominal \4scera. After 
a time they assume a more infectious character, infiltrating the soft 
parts with which they come in contact, and forming metastatic 
tumors in the liver and other ^dscera. 

These tumors are composed of a stroma and cells. The cells are 
large, of cuboidal shape, and often undergo fatty degeneration, when 
they become swollen. The proportion between the cells and the 
stroma, and the arrangement of the cells, vary in the different cases 
and in different parts of the same tumor (Fig. 238). 

The stroma may be abundant and the cells scattered irregularly, 
each cell in a little cavity of its own. The stroma may be abundant, 
but the cells are collected in masses as in a carcinoma. 

The cells are abundant and close together, but each cell is sur- 
rounded by a thin partition of connective tissue. The blood vessels 
are numerous, and the cells are arranged around them with some 
regularity. 

From the above description it will be seen that these tumors are 
of peculiar structure and perhaps do not really belong to the sarco- 
mata. 

Cysts of the mesentery are of occasional occurrence. They may 
be filled with chvle, with blood, or Avith serous fluid.' or mav be due 
to the echinococcus. 

Multiple cysts of the omentum may form by transplantation of 
papillary cyst-adenomata from the ovary. 

PARASITES. 

Ecliinococci can be formed in their regular way at any part of 
the visceral and parietal peritoneum, or be free in the peritoneal cav- 
ity. These cysts may be small, or so large as nearly to fill the ab- 
dominal cavity, 

Cysticerciis celhdosce may also be developed in the subperitoneal 
connective tissue. 

' Regarding cysts of the mesentery consult Weicliselbaum, Yircliow's Archiv, 
Bd. Ixiv., p. 145; Bramann, Archiv fiir klin. Chirurgie, Bd. xxxv., p. 201; HaJin, 
Berliner klin. Wochenschrift, June 6th, 1887, p. 408 ; Mobinson, British Medical 
Journal, January 31st, 1891. 



THE LIVEE. 



MALFORMATIONS. 

Congenital malformations of the liver are not common and are 
of little practical importance. The organ may be entirely wanting ; 
the lobes may be diminished or increased in number ; its f orin may be 
altered, so that it is rounded, flattened, triangular, or quadrangular. 
The gall bladder or gall ducts may be wanting ; the ductus choledo- 
chus may be double, both ducts emptying into the duodenum, or one 
emptjring into the duodenum, the other into the stomach. The single 
ductus choledochus may also empty into the stomach. Owing to 
abnormal openings in the diaphragm or the abdominal j)arietes, the 
liver may suffer displacement upward or forward. In congenital 
transposition of the viscera the liver is found on the left side, the 
stomach and spleen on the right side. 

Small, isolated bodies, having the same structure as the liver, have 
been a few times found in the suspensory ligament and in the lesser 
omentum. 

ACQUIRED CHANGES IN SIZE AND POSITION. 

As a result of tight lacing very marked changes are sometimes 
produced in the shape of the liver. By the narrowing of the base of 
the thorax the organ is compressed from side to side, and its convex 
surface is pressed against the ribs. In consequence of this there are 
found ridges and furrows on its convex surface. In consequence also 
of the circular constriction, a part of the right, and usually of the left 
lobe also, becomes separated by a depression. . Over this depressed 
and thinned portion of the hver the capsule is thick and opaque. In 
extreme cases the depressing and thinning reach such an extent that 
there is only a loose, ligamentous connection between the separated 
portion and the liver. 

A series of depressions are sometimes found on the up[)or surface 
of the right lobe of the liver, running from front to back, apparently 
caused by folds of the organ. 

Structural changes in the liver niav induce chanuvs in its size and 
43 



490 THE LIVER. 

shape. It may be increased in size by tumors, hydatid cysts, abscesses, 
fatty and amyloid degeneration, by congestion, and sometimes by 
cirrhosis, etc. 

It may be diminished in size by atrophy, by cirrhosis, by acute 
parench}Tiiatous degeneration, etc. 

Changes in the position of the hver are produced by alterations in 
its size, by pressure downward from the thoracic cavity and upward 
from the abdomen, by the constriction of tight lacing, by tumors or 
circumscribed serous exudation between the liver and diaphragm, by 
curvature of the spine. 

The liver is readily turned, by pressure from above or below, on 
its transverse axis. The transverse colon may be fixed above the 
liver so as to push it backward, downward, and to the right. There 
are a few cases recorded of dislocated and movable livers. These 
occurred in women who had borne children and whose abdominal walls 
were lax. With ascites it is not uncommon to find the liver quite 
movable. 

ANEMIA AND HVPER.EMIA. 

Ancemia of the liver may be general or partial. It may be due to 
general anaemia or to local disturbances of the circulation, such as 
swelling of the cells in parenchymatous or other degeneration, pres- 
sure of tumors, etc. The organ appears pale, often of slightly yellow- 
ish or brownish color. It may be harder than usual, and smaller. 

Hyperoemia of the liver is either an active or a passive process. 
In health the amount of blood in the liver varies at different times, 
being regularly increased during the process of digestion. When the 
digestive process is unduly influenced by the ingestion of spirits, 
spices, etc. , the hyperaemia assumes abnormal proportions, and when 
this is often repeated it may lead to structural changes in the organ. 
Severe contusions over the region of the liver sometimes cause a hj'per- 
semia, which may result in suppurative or in indurative inflammation. 
In hot climates and in malarious districts active and chronic hyper- 
semia of the liver are frequent and often cause structural lesions. 
In scurvy, also, the liver is sometimes congested. Cessation and 
suppression of the menses and of hsemorrhoidal bleeding may cause 
hypersemia of the liver. In aU these varieties of active congestion 
the liver is enlarged, of a deep-red color, and blood flows freely from 
its cut surface. 

The passive congestions of the liver are produced by some obstruc- 
tion to the current of blood in the hepatic veins. Valvular diseases 
of the heart, emphysema and fibrous induration of the lungs, large 
pleuritic effusions, intrathoracic tumors, angular curvature of the 
spine, aortic aneurisms pressing on the vena cava, and constrictions 



THE LIVER. 



401 



of the vena cava and of the hepatic veins, may all produce a chronic 
hypersemia of the liver. In all these cases, as the congestion affects 
principally the hepatic veins, we find the centre of each acinus con- 
gested and red while its periphery is lighter in color. This gives to 
the liver a mottled or nutmeg appearance {nutmeg liver). The liver 
cells in the centre of each acinus are frequently colored by little gran- 
ules of red or black pigment, and the cells at the periphery become 
fatty, so that the nutineg appearance is still more pronounced. A 
liver in this condition is usually of medium size, but may be smaller 
or larger than normal. 

^7 :\' •<' ,- V • •> * *"^''--''" " »■"«:»» ^«^ '■> 

a . -;"^- ./-''^ ■"• \- '• \^' * * /* 4. ^ •.%-•'- -.t %^. '■»">■:, 









fl,.. 




* •> 


e^ 


l>- 




*v ft ' 


*> * 



r>^ 



i^/"* 






'ojfr^ 




^ 









0— -S^iV 



^tt,/' 



• f ♦ 



Fig. 239.— Chronic Congestion of the Liver (nutmeg liver). 
This section shows complete atrophy of the liver cells at the centre of the lobule, a, dilated 
venacentrahs; ?>, dilated capillaries filled with blood; c, portal vein surrounded by connective tis- 
sue; (7, gall duct; e, atrophied liver cells; g, nearly normal liver tissue. 

When the congestion is long-continued the veins at the centre oi 
each acinus may become permanently dilated, the hepatic cells in 
their meshes become atrophied (Fig. •^liO), so that the centre of each 
acinus consists only of dilated capillanes or of these and new coniu\"- 
tive tissue ; or the dilatation and atrophy of the liver cells may. in 
circumscribed portions of the organ, involve the entire acinus. In 
long-continued congestion the liver is usually smaller than normal, 
and may be slightly roughened or uneven on the snrfacH^ : but it is 



49-2 . THE LIVER. 

sometimes enlarged. The peculiar nutmeg appearance may be very 
well marked, or it may not be e^ddent. the organ being of a dark-red 
color. 

WOUNDS, RUPTURE, AND HEMORRHAGE. 

JVounds of the liver ma}' induce haemorrhage, which, if life con- 
tinue, is foUowecl by inflammation. Serious wounds of the liver are 
usually fatal, but recovery may occur even after the destruction of a 
considerable portion of the organ. 

Rupture of the liver may be produced by severe direct contusions 
or by falls. It may be produced in children by artificial delivery. 
The rupture usually involves both the capsule and a more or less con- 
siderable portion of the liver tissue. It is commonh' accompanied by 
large haemorrhage, and is usuall}^ fatal. 

HcEmorrhage. — Extravasations of blood in the substance of the 
liver, or more frequently beneath the capsule, are found in new-born 
children after tedious or forcible labors. In adults hsemorrhage, 
except as the result of injury, is uncommon. Extravasations of 
blood are sometimes seen in malignant malarial fevers, especially in 
tropical climates ; in scurv}", purpura, and phosphorus poisoning ; 
and bleeding may occur in and about soft tumors, abscesses, and 
echinococcus cysts. It may also occur as a result of thrombosis of 
the hepatic vein. 

LESIONS OF THE HEPATIC ARTERY. 

The hepatic artery is in rare cases the seat of aneurisms which 
may attain a large size. Such aneurisms may displace the liver tis- 
sue, compress the bile ducts so as to cause jaundice, and may rupture 
into the stomach or abdomen. 

Owing to its abundant anastomoses, emboli of tlie branches of the 
hepatic artery usually induce no marked lesions, but they sometimes 
result in haemorrhagic infarctions. 

LESIONS OF THE PORTAL VEIN. 

Thrombosis, Embolism, and Inflammation. — Thrombosis of the 
branches of the portal vein may be produced by weakening of the cir- 
culation from general debility — marasmatic thrombi ; by pressure 
on the vessel from without, as in cirrhosis, tumors, gall stones, dila- 
tation of the bile ducts, etc. ; by injury ; by the presence of foreign 
materials within the vessel ; and as a result of inflammation of its 
wall, or of embolus. The thrombus may form in the vessels in the 
liver or be propagated into them from without. It may partially or 
entirely occlude them. The clot may become organized as a result of 
endophlebitis, and a permanent occlusion of the vessel ensue. If the 



THE LIVER. 493 

clot be a simple, non-irritating one, leading to occlusion, the conse- 
quences are usually more marked in the abdominal viscera than in 
the liver itself. The branches of the hepatic artery form, sufficient 
anastomoses to nourish the liver tissue and prevent its necrosis, even 
in complete occlusion of the portal vein ; and if occlusion occur slow- 
ly the organ may continue to perform its functions. But this oblite- 
rative form of thrombosis is usually attended by ascites, enlargement 
of the spleen, dilatation of the abdominal veins, and sometimes by 
haemorrhage from the stomach and intestines. 

In another class of cases, in addition to the local and mechanical 
effects of a thrombus, there may be necrotic changes and suppurative 
inflammation in the walls of the vessels or in the liver tissue about 
them. The thrombi are apt to soften and break down, and the frag- 
ments may be disseminated through the smaller trunks of the portal 
vein. In this way, by the distribution through the smaller vessels 
of a disintegrated thrombus from a large trunk, or by the introduc- 
tion into the branches of the portal vein of purulent or septic material 
from some of the abdominal viscera or from wounds, multiple foci of 
purulent inflammation in the portal vein, and multiple abscesses in- 
volving the liver tissue, may be produced. In many cases the pre- 
sence of bacteria may be detected in the inflammatory foci. 

These soft thrombi of the portal vein and the accompanying pyle- 
phlebitis and abscess may be caused in a variety of ways. Ulcera- 
tion of the intestines and stomach, abscesses of the spleen, suppurative 
inflammation of the mesentery and mesenteric glands, inflammation 
and ulceration of the bile ducts from gall stones, inflammation of the 
umbilical vein in infants, may all induce thrombi in their respective 
veins, which may be propagated to the portal vein or may give rise 
to purulent or septic emboli. Two cases are recorded in which a fish 
bone in the portal vein induced suppurative inflammation in that 
vessel. One of these cases, occurring in Bellevue Hospital in 18G7. was 
reported by Dr. E. G. Janeway. Male, 47 ; dying, after a four weeks' 
illness, in a typhoid condition, with lesions of sero-fibrinous peritoni- 
tis and chronic diffuse nephritis. There were numerous small ab- 
scesses in the right lobe of the liver, two in the left lobe. The left 
division of the portal vein contained a firm red and white clot over 
an inch long ; the right division was lined with a, firm thrombus. 
The walls of the vein were thickened and contained purulent fluid. 
A fish bone, two inches long, its centre covered by a thrombus. lay 
half in the mesenteric and half in the portal vein. 

In certain cases of thrombosis and iuflannnation of xhc jHntal 
vein the cause cannot be discovered. 

In infants inflammation of the umbilical vein may tiot only induce 
inflammation of the portal vein and abscesses in the liver, Inu n\ultiple 



494 THE LIVER. 

abscesses in various parts of the body, and acute peritonitis may be 
induced. 

Rupture of the Portal Vein, with fatty degeneration of its 
walls, has occurred in a few instances. 

Chronic Endophlehitis, with atheroma and calcification, may 
occur in the walls of the portal vein, giving rise to thrombosis. 

Dilatation of the Portal Vei7i, either uniform or varicose, may 
occur in various parts of the vessel or its branches. It may be caused 
by destruction of the liver capillaries in cirrhosis, or by occlusion of 
the vein by thrombi, tumors, etc. 

THE HEPATIC VEINS. 

The hepatic veins present lesions similar to those of the portal vein 
and its branches, but they are much less frequent. They may be 
dilated by obstruction to the passage of venous blood into the heart. 
They may be the seat of acute and chronic inflammation, and soft 
thrombi and suppurative inflammation may be produced by abscesses 
in the liver. 

ATROPHY OF THE LIVER. 

Atrophy of the liver may affect the entire organ or be confined to 
some part of it. General atrophy may occur in old age as a senile 
change, or may be induced by starvation or chronic exhausting dis- 
eases. The organ is diminished in size, is usually firm, and the acini 
appear smaller than usual. Microscopically the change is seen to be 
due to a diminution in size of the liver cells, and hand-in-hand with 
this there occurs frequently an accumulation of pigment granules 
within the atrophied cells. The cells may entirely disappear over 
circumscribed areas, leaving only shrivelled blood vessels and con- 
nective tissue ; or, in some cases, there may be an increase of con- 
nective tissue in connection with the atrophy of the cells. When 
much pigment is formed in the cells the lesion is often called pigment 
atrophy. 

Essentially the same changes may occur in circumscribed portions 
of the liver, as the result of pressure from new connective tissue in 
cirrhosis, from tumors, hydatids, amyloid cJegeneration, gall stones, 
etc. In atrophy from pressure the liver cells are apt to become very 
much flattened and squeezed together as they diminish in size. 

DEGENERATIVE CHANGES. 

Acute Degeneration ; Parenchymatous Degeneration (Cloudy 
Swelling). — In a variety of acute and infectious diseases — pneumo- 
nia, typhoid and typhus fevers, scarlatina, variola, diphtheria, ery- 
sipelas, yellow fever, septicaemia, and in certain cases of acute anse- 



THE LIVEK. 495 

mia and phosphorus poisoning — the liver is somewhat swollen and, 
on section, of a dull yellowish-gray color, looking somewhat as if it 
had been boiled. It contains less blood than usual, and the outlines 
of the lobules are indistinct. Microscopical examination shows the 
lesion to consist of a swelling of the liver cells and an accumulation 
in them of moderately refractile, finer and coarser albuminous gran- 
ules. Those granules may disappear and the cells return to their 
normal condition, or, as is frequently the case, they may pass into 
a condition of fatty degeneration. Very frequently fatty and paren- 
chymatous degenerations are associated together. 

Small areas of necrosis of liver cells may be found in certain 
acute infectious diseases. 

Fatty Infiltration. — In the normal human liver there is usually 
a certain amount of fat in the liver cells, and this amount varies con- 
siderably under different conditions. 

The gross appearance of pathological fatty livers varies a good 
deal, depending upon the amount and distribution of fat and its as- 
sociation with other changes. If the lesion is uncomplicated and 
considerable the organ is increased in size, the edges rounded, the 
consistence firm, the color yellowish, and the cut surface greasy. 
The lobules are enlarged and their outlines usually indistinct, and 
the blood content diminished. The liver is increased in weight. If 
the amount of infiltration be moderate the outlines of the lobules 
may be more distinct than usual and the centres appear unusually 
red. This is due to the fact that the accumulation of fat usually 
commences in the periphery of the lobules and progresses toward 
the centre, so that the centre appears darker by contrast with the 
fatty periphery. The lesion may be uniform throughout the organ 
or it may occur in patches. In the latter case the liver has a mot- 
tled appearance, irregular yellowish patches alternating with the 
brownish-red, unaffected portions. 

Fatty infiltration is often associated with chronic congestion {nut- 
meg liver), with cirrhosis and amyloid degeneration ; the picture 
may then present considerable complexity. Fatty livers may be 
stained brown or greenish with bile pigment. 

Microscopically the liver cells are seen to contain larger and 
smaller droplets of fat (Fig. 240), and frequently large drops of fat 
occupy nearly the entire volume of the cell, so that the protoplasm 
may be visible only as a narrow, nucleated crescent at one side, or 
it may disappear altogether (Fig. 241). The microscopical ap}H\n-- 
ances of course vary, depending upon the degree of intilt ration and 
the association with other lesions. 

Fatty infiltration of the liver may occur as a result of excessive 
ingestion of oleaginous food ; in chronic alcohol. }>hosphorus, and 



496 



THE LIVER. 



arsenic poisoning ; in certain exhausting diseases accompanied hy 
malnutrition, as in pulmonary phthisis, chronic dysentery, etc. ; and 
under a variety of conditions which we do not understand. 

Fatty Degeneration. — In this condition, which in many cases 
cannot be morphologically distinguished from fatty infiltration, the 
fat is believed to be formed by a transformation of the protoplasm 




Fig. 240.— Fatty Infiltration of Liver Cells. 



of the liver cells. The fat droplets are, for the most part, very 
small and abundant, though this is not constant. Fatty degenera- 




'^^^'•-'^SA^'^" 



Fig. 241.— Fatty Infiltration op Liver. 
Portion of the periphery of a lobule. 



tion of the liver cells frequently follows, and is associated with, 
cloudy swelling under the varpng conditions in which this occurs, 
or it may appear in profound ansemia and in acute phosphorus and 
arsenic poisoning. 

Amyloid Degeneration (Waxy Liver).— In the liver amyloid 
degeneration may be general or local ; so extensive as to give the 



THE LIVER. 



Vj7 



organ very characteristic appearances, or so slight as to be unrecog- 
nizable without the aid of the microscope. It may be associated 
with other lesions. When the change is extensive and general the 
liver is enlarged sometimes to more than twice its normal size ; the 
edges are thickened and rounded ; the surface smooth ; the tissue 
tough, firm, inelastic, more or less translucent, and of a brownish- 
yellow color. The lobular structure may be more or less indistinct, 
or it may become very evident by an associated fatty degeneration 
of the peripheral or central cells of the lobules. The translucency 
and peculiar appearance of the tissue may be best seen by slicing off 
a thin section and holding it up to the light. When the lesion is 



■ ■^rm;?^,. 




's.'».,'<fT.".>'-.^' '^' 

Fm. 242.— Amyloid Degeneration of the Ljveb. 
The degenerated walls of the vessels are stained red. 

less considerable the liver may be of the usual size, and may feel 
harder than normal, and here and there a translucent mottlinc; mav 
be evident, or the degeneration may be apparent only on the addi- 
tion of staining agents. When, as is frequently the case, it is as- 
sociated with cirrhosis, the liver may be small and nodular, and the 
appearance of the cut surface will vary greatly, depending upon xhc 
character of the cirrhotic change and the presence or absence of fat. 
This degeneration usually commences in the walls of the intra- 
lobular blood vessels, causing tliem to become thickened and translu- 
cent. The liver cells are sipieezed by the thickening of the vessels 
and may become partially or completelv atrophied (Fii;-. 'H'i). 
it ^ ^ ^ 



498 THE LIVER. 

It is stated by some observers that the hver cells maj also become 
waxv, but we have been unable to find them unmistakablv thus 
changed. The liver cells not infrequently undergo fatty metamor- 
phosis. Amyloid degeneration may also involve the interlobular ves- 
sels, and in advanced stages larger and smaller areas of Hver tissue 
may be nearly or completely converted into the dense, refractile sub- 
stance which in its arrangement but obscurely represents the group- 
ing and structure of the affected lobules. l!^ot infrequently atrophic 
or fatty liver cells are seen scattered singly or in clusters through the 
amyloid masses. In the affected regions the blood content of the 
liver is considerably diminished, or it may be nearly entirely absent. 

Amyloid degeneration of the liver is usually associated ^^dth a 
similar lesion of other organs, such as spleen, kidneys, intestines, etc.. 
although it may occur in this organ alone. It usually occurs in 
cachectic conditions, as in chronic phthisis ; in chronic suppurations, 
especially of the bones ; in syphilis, and sometimes in malarial poison- 




FiG. 243. — Pigmentation of the Liver in ^Ialakiai, Fever. 
The pigraent in this specimen was contained in cells lying within the liver capillaries. 

ing. It occasionally occurs unassociated vith any of these con- 
ditions. 

PIGMENTATION OF THE LIVER. 

As a result of severe malarial poisoning a variable amount of 
brown, black, or reddish pigment is often found in the blood. This is 
usually mostly taken up by the leucocytes and deposited in various 
parts of the body, chiefly in the hver, spleen, and marrow of the 
bones. In the liver it is usually found enclosed in variously shaped 
cells which lie especially in the blood vessels, but sometimes in the 
tissue between them (see Fig. 243). The liver cells frequently con- 
tain bile pigment, but usually are free from the melanotic pigTuent 
characteristic of this malarial condition. As the result of tliis ac- 
cumulation of pigment the liver may have a dark reddish-brown, an 
olive-brown, or black color (sometimes called bronze liver). This 
condition may be associated with various other lesions of the liver, 
depending upon the nature and extent of which the organ will present 



THE LIVER. 400 

a great variety of appearances. Thus there may be fatty or waxy 
degeneration, cirrhosis, chronic congestion, etc. 

Pigment may be found in the connective tissue along the jjortal 
vessels similar in character to that which occurs in the lungs from 
the inhalation of coal dust. This inhaled pigment, according to the 
researches of Weigert, doubtless finds access to the blood and is de- 
posited in the liver as it is in the spleen and hepatic lymph nodes. 

Pigmentation of the liver cells, which is to a certain extent nor- 
mal, may be greatly increased as a result of atrophy, localized haemor- 
rhage, and of obstructive jaundice. ^ 

ACUTE YELLOW ATROPHY OF THE LIVER. 

This disease is characterized anatomically by a rapid diminution 
in the size of the liver as the result of a granular and fatty degenera- 
tion and disintegration of the liver cells. The liver, sometimes with- 
in a few days, may be reduced to one-half its normal size. On open- 
ing the abdominal cavity the organ may be foiuid lying, concealed 
l)y the diaphragm, close against the vertebral column. The amount 
of diminution and the general appearance of the affected organ de- 
pend to a considerable extent upon its previous condition — i.e.. 
whether or not it was the seat of other lesions — as well as . upon the 
degree of degenerative change. In general, if the lesion is well 
marked, the liver is small, flabby — sometimes almost fluctuating — 
and the capsule wrinkled. On section the cut surface may show bat 
little trace of lobular structure, but presents an irregular mottling 
Avith gray, ochre-yellow, or red ; sometimes one, sometimes another 
color preponderating. 

Microscopical examination shows varying degrees of degeneration 
and destruction of the liver cells. Most evidently in those parts which 
have a grayish appearance, the outlines of the cells are preserved 
and the protoplasm is filled with larger and smaller granules. In 
the yellow portions the outlines of the liver cells may be preserved, 
and they may contain varying quantities of larger and smaller fat 
droplets and granules of yellow pigment. Or the cells may be com- 
pletely disintegrated, and in their place irregular collections of fat 
droplets, pigment granules, red and yellow crystals, and detritus : 
only the connective tissue and blood vessels of the original liver tis- 
sue remaining. The red areas may show nearly complete absence of 
liver cells and cell detritus, and sometimes irregular rows of cells 
which are variously interpreted as being new-formed gall ducts or 
proliferated liver cells. In these areas it a})pears to be. in part at 



' The distribution aud amount of the pis^nient may be well seen by .^tainin^ir thin 
sections with eosiu and mounting in eosin-glyceiin or balsam. 



500 THE LIVER. 

least, the blood contained in the vessels "which imparts the red color. 
Sometimes the interstitial tissue is infiltrated with small spheroidal 
cells resembling leucocytes. Crystals of leucin and ty rosin are 
sometimes found intermingled "wath the cell detritus. In some cases 
the liver is not diminished in size. 

These lesions of the liver are frequently associated with enlarge- 
ment of the spleen and parenchymatous degeneration of the kid- 
ney and of the heart muscle. Multiple hsemorrhages may occur in 
the gastro-intestinal canal, kidneys, bladder, and lungs. There is 
usually marked jaundice. Rod-shaped bacteria and micrococci have 
been found in the Hver, but their significance is doubtful ; we have 
not been able to find them in the cases which we have examined. 
The cause of the disease is unknown, and it is doubtful whether it is 
a disease primarily of the liver or an acute infectious disease with 
local lesions. It is not unlikely that more than one form of lesion is 
grouped under this heading. 

INFLAMMATION OF THE LIVER. 

Acute Hepatitis (Purulent Hepatitis ; Abscess of the Liver). — 
Purulent or suppurative inflammation of the liver may be the result 
of injury ; it may be secondary to inflammation of the gall ducts or 
the branches of the portal vein. It may occur as the result of the 
presence of tumors, parasites, or from propagation of an inflam- 
matory process from without, as in ulcer of the stomach with ad- 
nesions to the liver and secondary involvement of the latter. It is 
often directly due to the introduction into the organ, through the 
blood vessels or gall ducts or other^^^ise, of bacteria. Purulent in- 
flammation in the liver almost always results in abscess. 

Large abscesses of the liver may be traumatic, but are, for the 
most part, due to unknown causes. They are not infrequently as- 
sociated with dysentery, and may then be due to the conveyance 
through the veins of septic material from tlie intestinal ulcers. They 
may be due to the presence of the amoeba coli. They occur most fre- 
quently in tropical climates, but are not very uncommon in the tempe- 
rate zones. They are usually single, but there may be several of them. 
They are sometimes so large as to occupy a large part of a lobe. 
They are most frequent in the right lobe, but may occur in any part 
of the organ. They tend to enlarge, and as they do so they ap- 
proach the surface of the liver. Here the contents of the abscess 
may be discharged into the peritoneal cavity. More frequently, 
however, as they approach the surface, a localized adhesive peritoni- 
tis ensues, so that the hver becomes bound to adjacent parts, and 
thus the abscess may open into the pleural cavity, or, owing to a 
secondary pleurisy with adhesions, into the lung tissue. They may 



THE LIVER. OOI 

open into the pericardium. They may open externally tdrough the 
abdominal wall ; into the stomach, duodenum, colon, or j)elvis of the 
right kidney ; into the hepatic veins, portal vein, vena cava, or gall 
bladder or gall ducts. 

The early stages in the formation of large abscesses of the liver 
are but httle known. It is probable, however, that in many cases 
they are the result of the confluence of smaller abscesses. Their 
contents, usually bad smelling, may be thick and yellow like ordi- 
nary pus, but more commonly they are thin, reddish-brown or 
greenish in color from admixture with the pus of blood, gall pig- 
ment, and broken-down liver tissue. Microscopical examination 
shows the contents to consist of fluid with pus cells, more or less de- 
generated blood, degenerated liver cells, fragments of blood vessels, 
and pigment granules and crystals. The walls of the abscess are 
usually ragged, shreds of necrotic liver tissue hanging from the 
sides. Microscopical examination of the liver tissue near the ab- 
scess shows infiltration with pus, flattening of the liver cells from 
pressure, cloudy swelling, and necrosis of those lying along the 
cavity. Bacteria or the amoeba coli may be present. Liver ab- 
scesses due to the presorice o.'* the amoeba coli have certain peculiari- 
ties, concerning which reLcrence is made to the studies of Council- 
man and Lafleur, "Amoebic Dysentery, ^^ Johns Hopkins Hospital 
Keports, vol. ii., p. 490, 1892. 

After the discharge of the contents of the abscess or without 
this if it be not very large, granulation tissue may form in the wall 
of the cavity and a fibrous capsule be produced, enclosing the con- 
tents, which become thickened and often calcareous, and in this 
condition may remain for a long time. Or the connective-tissue 
walls may approach one another and join, forming a fibrous cica- 
trix at the seat of the abscess. 

Several large abscesses may, one after another, heal in this way 
after evacuation of their contents, with little diminution in the size 
of the liver. ' 

Abscesses of the liver accompanying inflammation of the portal 
vein and gall ducts are considered elsewhere in this section. 

Small multiple metastatic abscesses are not infrequent in pyro- 
mia, and are called pyaimic abscesses. In these abscesses we can 
readily study the various stages of formation. Suppurative pro- 
cesses in any part of the body— in the head, upper and lower ex- 
tremities, etc. — may favor the production of the noxious materials, 
which in most cases are probably associated with bacteria, or are 



1 Eddwhls, "Dysentery and TTepatic Abscess with Amoeba Coli." Proceediugs of 
the New York Pathological Society, 1892. 

44 



502 



THE LIVER. 



bacteria themselves. These, entering the circulation, may pass the 
heart and pulmonary capillaries, with or without inducing lesions 
in the lungs, and, lodging in the vessels of the liver, induce circum- 
scribed necrosis of the liver tissue and suppurative inflammation. 
Under these conditions we may find on a section of the liver larger 
and smaller yellowish or grayish spots, the larger of which may be 
soft and present the usual characters of abscesses. The smaller, 
which may not be larger than a pin's head, may present the usual 



G r 







Fig. 244.— Chronic Interstitiai, HEPATirrs. 
a, new-formed connective tissue; b, dilated blood vessels of the new tissue; c, gall duct;. 
d, parenchyma of liver. 

consistence of liver tissue with the lobular structure still evident ; 
others may be softer, more yellow, and surrounded by a zone of 
hypersemic liver tissue. Microscopical examination of the earlier 
stages often shows the blood vessels filled with micrococci, scattered 
and in masses. Around these the liver cells are found in various 
stages of necrosis ; in many the nuclei do not stain and the bodies 
are very granular, or the entire cell is broken down into a mass of 
detritus. About these necrotic islets of liver cells pus cells collect 



THE LIVER. 503 

and often form a zone of dense infiltration. Thus, by the increase of 
pus cells and the necrosis of liver tissue, small abscesses are formed 
whose contents are intermingled with greater or less numbers of bac- 
teria, which seem to increase in number as the process goes on. By 
the confluence of small abscesses larger ones may be formed. 
Death usually ensues, however, before the abscesses attain a very 
large size. 

Clwonic Interstitial Hepatitis (Cirrhosis). — The most marked 
result of chronic interstitial hepatitis is the formation of new connec- 
tive tissue in the liver. The character, amount, and distribution of 
the new tissue vary greatly in different cases. Secondarily there 
are usually marked changes in the liver cells and in the blood ves- 
sels and gall ducts. The new tissue is most commonly formed and 
most abundant in the periphery of the lobules along the so-called 
capsule of Glisson, but it may extend into the lobules between the 
liver cells. It may surround single lobules, or more frequently larger 
and smaller groups of lobules (Fig. 244). It may occur in broad or 
narrow, irregular streaks or bands. It is frequently more abundant 
in one part of the liver than in another. The new-formed tissue 
tends to contract, and thus compromise by pressure the enclosed islets 
of liver tissue, causing them to project, in larger and smaller nod- 
ules, from the surface of the organ. The liver cells may be flattened 
or atrophied from pressure ; or, from interference with the portal cir- 
culation, they may atrophy or become fatty ; or they may become 
colored with bile pigment. The varied appearances which cirrhotic 
livers present to the naked eye depend largely upon the amount and 
distribution of the new connective tissue and upon the secondary 
changes in the liver cells. 

In some cases the liver is enlarged, sometimes so much so as to 
weigh nine or ten pounds, the surface smooth or slightly roughened ; 
in other cases it may be finely or coarsely nodular on the surface. It 
may be smaller than normal, sometimes very small indeed, so as 
to weigh only one or two pounds. The surface may then be very 
rough and uneven from the projection of larger antl smaller nodules 
of liver tissue, or it may be quite smooth ; or the organ may be 
greatly distorted by the contraction of large bands or masses of new 
connective tissue. In section through cirrhotic livers the new tis- 
sue may not be visible to the naked eye, or it may appear as gray- 
ish, irregular streaks, or bands, or patches, often sharply outlined 
against the dark-red, or brown, or yellow, or greenish-yellow paren- 
chyma. 

On microscopical examination the new connective tissue is found 
in some cases loose in texture and containing many variously shajxHl 
cells ; or it may be dense and contain comparatively few colls ; it is 



504 



THE LIVER. 



usually quite vascular. Not infrequently, when occurring largely 
between the lobules, it will be f oiuid to have encroached more or less 
upon their peripheral portions. Very frequently there are found in 
the new connective tissue cylindrical ducts lined with cuboidal cells, 
and resembling gall ducts (Fig. 245, c) ; or irregular rows of more 
or less cuboidal or polyhedral cells, which look somewhat like the lin- 
ing cells of the medium-sized gall ducts, or like altered liver cells. 
The branches of the hepatic and portal veins, particularly the latter, 
often become obliterated by pressure from the new connective tissue 
or from chronic thickening of their walls, so as to seriously interfere 









^^"X 










^% 






'Cu 



'a 




Fig. 245.— Chronic Interstitial Hepatitis. 

Showing a portion of the section shown in Pig:. 244, but more highly magnified, a. portions of 
hver lobules; 6, new-formed connective tissue; c, gall ducts, apparently new formed; d, blood 
vessels in the new tissue. 



with the function and nutrition of the liver cells. The bile ducts 
also may become obliterated, or there may be catarrhal inflammation, 
especially of the larger trunks. The branches of the hepatic artery 
are much less liable to alterations than the other vessels. The cap- 
sule of the hver is usually thickened, either uniformly or in irregular 
patches ; or its surface may be roughened by larger and smaller 
papillary projections. The liver is frequently bound to the diaphragm 
or other adjacent organs by connective-tissue adhesions. Amyloid 
and fatty degeneration may be associated with cirrhosis. Cirrhotic 



THE LIVEK. oOo 

livers frequently show an unusual number of leucocytes in the blood 
vessels. 

The obstruction to the portal circulation induced by cirrhosis 
usually gives rise to a number of secondary lesions, since collateral 
circulation is rarely established in sufficient degree to afford much 
relief. The hsemorrhoidal and vesical veins may be greatly enlarged, 
and also veins of communication between Glisson^s capsule and the 
diaphragmatic veins. 

In rare cases a very peculiar dilatation of the cutaneous veins 
about the umbilicus is observed. The enlarged veins form a circular 
network around the umbilicus, or a pyramidal tumor alongside of it, 
or all the veins of the abdominal wall, from the epigastrium to the 
inguinal region, are dilated. This condition is said to be produced 
by the congenital non-closure and subsequent dilatation of the umbil- 
ical vein and its anastomoses with the internal mammary, epigastric, 
and cutaneous veins. According to Sappey, it is not the umbihcal 
vein which is dilated, but a vein which accompanies the ligamentum 
teres. 

There is very frequently also a dilatation of the veins of the 
abdominal wall, which has a different cause. It is produced by the 
pressure of the fluid of ascites on the vena cava, and is found with 
ascites from any cause and with abdominal tumors. 

Ascites is the most common secondary lesion of cirrhosis. It 
usually begins at an early stage of the disease, and is apt to increase 
constantly. It usually precedes oedema of the feet, but botli may 
appear at the same time. This fluid is of a clear yellow or brown, 
green or red ; it is sometimes mixed with shreds of fibrin, and more 
rarely with blood. The peritoneum remains normal, or becomes 
opaque and thick, or there may be adhesions between the viscera. 

The spleen is very frequently enlarged, and the enlargement may 
be very considerable. When it is not increased in size this seems 
usually due to previous atrophy of the organ, or to fibrous thickening 
of its capsule, or to haemorrhages from the stomach and bowels occur- 
ring just before death. 

The stomach and intestines are often secondarily affected by the 
obstruction to the portal circulation. Profuse luiemorrhage from the 
stomach and intestines may occur and sometimes cause sudden death. 
The mucous membrane is then found pale, or congested, or with 
hsBmorrhagic erosions. Sometimes the blood is intiltratod in the 
coats of the stomach and intestines. The mucous membrane of the 
stomach, and of the entire length of the intestines, is frequently the 
seat of chronic catarrhal inflammation, and is sometimes uniformly 
and intensely congested and coated with nuicus. In other cases both 
the mucous and muscular coats are pale, but very markedly thickened. 



506 



THE LIVER. 



Cirrhosis of the liver is not infrequently accompanied hy chronic 
diffuse nephritis. 

. The causes of cirrhosis are imperf ecly understood. It is a disease 
of adult life, but exceptionally occurs in children. In adults it seems 
in many cases to be directly dependent upon the continued ingestion 
of large quantities of strong alcoholic liquors. It very rarely occurs 
as a result of beer drinking. There are many cases of cirrhosis for 
ivhich no cause can be discovered. It is probable that in certain cases 
a degeneration of circumscribed areas of liver parenchyma precedes 









f 



L^ 



^-s 



n 



f - 





1 




FiG- 246 — Syphilitic Hepatitis. 
A so-called miliary gumma from the liver of a child with congenital syphilis. 

and probably determines the new formation of connective tissue. 
Welch ^ has described the occurrence of small circumscribed areas of 
fibrous tissue in the liver, replacing liver cells and containing coal 
pigment. This rare lesion he has called cirrhosis hepatis anthra- 
cotica. 

Syphilitic Hepatitis. — Chronic interstitial inflammation of the 
liver very frequently results from syphilitic infection, either congeni- 
tally or in the later stages of the acquired form. It may occur in a 

^ Welch, " Cirrhosis hepatis anthracotica," Johns Hopkins Hospital Bulletin, Febru- 
ary and March, 1891. 



• THE LIVER. 507 

diffuse manner, new connective tissue being formed either between 
the lobules, or within them between the rows of liver cells. The new 
tissue may be rich in cells, or dense and firm. This form is fre- 
quently seen in children, and cannot be distinguished, either macro- 
scopically or microscopically, from similar forms of interstitial he- 
patitis from other causes. 

In other cases, particularly in children, there may be numerous 
small gummata (so-called miliary gummata) scattered through the 
liver, together with more or less new connective tissue (Fig. 246). In 
adults gummata are usually larger, varying in size from that of a 
pea to a hen's Qgg, and may be surrounded by larger and smaller 
irregular zones of ordinary connective tissue (Fig. 247). In still 




Fig. 247.— Gumma of Liver. 

a, cheesy centre; 6 fibrous periphery; c, small-celled peripheral infiltration; d, portions of live 
lobules. 

other cases in adults we find larger and smaller dense, irregular 
bands or masses of connective tissue running through the liver, 
drawing in the capsule and often causing great deformity of the 
organ. These bands and masses of new tissue may or may not en- 
close gummata, either large or small. These deforming cicatrices, 
either with or without gummata, are very characteristie of syphilitic 
inflammation of the liver. 

This, like the simple interstitial iiitlainmation of the liver, may be 
associated with fatty and waxy degeneration, and with atrophy of 
the parenchyma from pressure. 

Tubercular Hepatitis. — This lesion, which is usually secondary 
to tubercular inflammation in some other part of the body, or a part 



508 THE LIVER. 

of acute general miliary tuberculosis, is most frequently characterized 
by the formation of larger and smaller miliary tubercles, which may 
be either within or between the liver lobules or in the walls of the 
bile ducts. Many of the tubercles are too small to be seen with the 
naked eye ; others may be just visible as grayish points ; still others 
may be from one to three mm. in diameter, with distinct yellowish- 
white centres. Microscopical examination shows considerable varia- 
tion in the structure of the tubercles in different cases, as well as in 
the same liver. Some of them, usually the smaller ones, consist 
simply of more or less circumscribed collections of small spheroidal 
cells, which are not morphologically distinguishable, so far as the 
form and arrangement of the cells are concerned, from simple inflam- 
matory foci, or from the diffuse masses of lymphatic tissue which 
occur normally in the liver. 

In other forms we find a well-marked reticulum with larger and 
smaller spheroidal and polyhedral cells, with or without giant cells. 
In still other forms there is more or less extensive cheesy degenera- 
tion. The larger forms are conglomerate, being composed of several 
tubercle granula joined together to foxm a single nodular mass. The 
liver cells at the seat of the tubercle are destroyed, and the interstitial 
tissue and blood vessels either destroyed or merged into the tubercle 
tissue. In the periphery of the tubercles the liver cells may be in a 
condition of coagulation necrosis, and the tissue round about may be 
infiltrated ^vith small spheroidal cells. There is in some cases a new 
formation of gall ducts or of structures which resemble these, and 
which in transverse sections look considerably like giant cells. Tu- 
bercle bacilH, frequently in small numbers, but often in great abun- 
dance, may be found within the tubercles. 

Tuberculosis of the liver may be associated with cirrhosis, waxy 
and fatty degeneration. 

Much more rarely than the above form there are found in the fiver 
more or less numerous scattered tubercular masses from the size of a 
pea to that of a walnut or larger, with cheesy centres and usually a 
new growth of connective tissue in the periphery. These so-called 
solitary tubercles of the liver may be softened at the centres. Tu- 
bercular inflammation of the gall ducts may give rise to numerous 
scattered, cheesy nodules, as large as a pea or larger, which may be 
softened at the centre and stained yellow with bile. This lesion is 
rare and seems to be more frequent in children than in adults. 

Perihepatitis. — Acute inflammation of the serous covering of 
the liver, with the formation of fibrin, may occur as a part of acute 
general or localized peritonitis, and over the surface of abscesses, 
tumors, hydatids, etc. , of the organ, when these lie near or approach 
the surface ; or it may be secondary to acute pleurisy. 



THE LIVER. 509 

Chronic perihepatitis, resulting in the thickening of and forma- 
tion of new connective tissue in and beneath the capsule of the liver, 
may be secondary to an acute inflammation of the capsule, or it may 
be chronic from the beginning and associated with chronic pleurisy, 
chronic peritonitis, and cirrhosis. In this way more or less exten- 
,sive adhesions of the liver to adjacent structures may be formed ; 
or, by contraction of the new-formed connective tissue, consider- 
able deformity of the liver may be produced. The capsule is some- 
times uniformly thickened, sometimes the new tissue occurs in more 
■or less sharply circumscribed patches. The surface is sometimes 
roughened from little, irregular projecting masses of connective 
tissue. Microscopically the new-formed tissue is usually dense and 
firm, but it may be loose in texture and contain many cells. Not in- 
frequently bands or masses of connective tissue run inward from 
the thickened capsule between the superficial lobules, causing local- 
ized atrophy of the parenchyma. 

Hyperplasia of Lymphatic Tissue in the Liver. — In some 
forms of leukaemia and pseudo-leukaemia the liver is not infrequently 
enlarged and soft and besprinkled with small white spots, or streaked 
with narrow whitish, irregular bands, or of a diffuse gra^'ish color. 
Microscopical examination shows this change to be due to an accu- 
mulation of cells resembling leucocytes, either along the portal vein, 
or diffusely through the liver tissue, or in small circumscribed inasses. 
The amount of accumulation of these small cells varies much, but is 
sometimes so great as to seriously compromise the liver cells. The 
origin of these new cells is not yet definitely known. They may be> 
and doubtless in part are, brought to the organ through the portal 
vein ; but they may, in part at least, be formed in the liver itself, 
possibly from the capillary endothelium. 

In typhoid fever, small-pox, scarlatina, diphtheria, and measles 
small circumscribed masses of cells resembling leucocytes are some- 
times found in the liver, Ij^ing in the meshes of a delicate reticular 
tissue. These are sometimes called miliary lymphomata ; but it 
should be remembered that small masses of lymphatic tissue nor- 
mally occur in the liver, and that as, under the above conditions, an 
hyperplasia of the lymph nodes and spleen is wont to occur, these 
so-called lymphomata are very probably normal structures, which 
have become more prominent under the conditions of disease owing 
to an acute inflammatory condition induced by absorbed ptomaines. 

TUMORS OF THE LIVER. 

Tumors of the liver may be primary or secondary ; tlie latter are 
most common. 

Cavernous Angioniata. — Those tumors, usually small, from five 



510 THE LIVER. 

to fifteen mm. in diameter, are most common in elderly persons 
and are of no practical significance. They may be situated at the 
surface or embedded in the organ, and are of a dark-red color ; 
sometimes sharply circumscribed by a connective-tissue capsule, 
sometimes merging imperceptibly into the adjacent liver tissue. 
Microscopically they consist of a congeries of irregular cavities (Fig. 
126, page 260) filled with blood and frequently communicating freely 
w^ith one another. The walls of the cavities consist of connective 
tissue, often containing small blood vessels, and are sometimes thick, 
sometimes thin. They are believed to be formed by dilatation of 
the liver capillaries, with subsequent thickening of their walls and 
atrophy of the adjacent liver cells. 

Small fibromata and Upomata have been described, as also fibro- 
neuromata of the sympathetic. 

Adenomata of the liver are of not infrequent occurrence. They 
are sometimes small and circumscribed, sometimes very large and 
multiple. They present two tolerably distinct types of structure. 
In one form the tissue presents essentially the same structure as nor- 
mal liver tissue, except that the arrangement of the cells is less uni- 
form and the cells are apt to be larger. They look like little islets of 
liver tissue, sometimes encapsulated and sometimes not, lying in the 
liver parenchyma. In the other form the cells are less like liver 
cells, are frequently cylindrical, and are arranged in the form of 
irregular masses of tubular structures with more or less well-de- 
fined lumina. These tumors are sometimes large and multiple, and 
in one case described by Greenfield there were metastatic tumors 
in the lungs. These tubular adenomata are in some cases so closely 
similar to some of the carcinomata as to be scarcely distinguishable 
from them, and seem, indeed, to merge into them. 

Carcinomata are the most common and important of the liver 
tumors, and may be primary or secondary. Primary carcinomata of 
the liver are probably developed from the epithelium of the gall 
ducts, and in some cases are arranged along the larger trunks. 
Their cells are usually polyhedral, sometimes cylindrical, and may 
be arranged irregularly in alveoli or form more or less well-defined 
tubular structures. 

Secondary carcinomata of the liver, which are by far the most com- 
mon, are most frequently due to the dissemination in the organ of 
tumor cells from carcinomata of the stomach, intestines, pancreas, or 
gall bladder. But they may be the result of metastases from the 
mamma, oesophagus, uterus, and various other parts of the body. In 
secondary carcinomata the cells resemble more or less closely the 
type of those forming the primary tumor. 

The form in which the carcinomatous nodules in the hver present 



THE LIVER. oil 

themselves is subject to considerable variation. Sometimes they are 
single, but more often multiple ; they may be very large, or so small 
as to be scarcely visible to the naked eye ; very frequently numerous 
small nodules are grouped in the periphery of a larger cancerous 
mass. They are sometimes deeply embedded in the liver, sometimes 
they project from the surface. The liver is frequently enlarged, 
sometimes enormously so. The nodules are usually whitish or 
yellowish or pink in color, but they are often the seat of haemor- 
rhages, and may become softened at the centre, forming cysts filled 
with degenerated tumor tissue which is often mixed with blood. The 
nodules are sometimes hard, sometimes soft and almost diffluent. 
Fatty degeneration is frequent, and may be evident to the naked eye 
in the form of yellowish streaks or patches on the cut surfaces. 
Owing to the degeneration and partial absorption of the central por- 
tions of the tumors, the nodules on the surface frequently present a 
shallow depression at the centre. The tumors may be sharply out- 
lined against the adjacent liver tissue, or may merge imperceptibly 
into it. They may be so large or numerous as to occupy the greater 
part of the enlarged organ. The liver tissue in their vicinity shows 
flattening and atrophy of the liver cells from pressure, and there may 
be infiltration with small spheroidal cells. The tumors may press 
upon the portal vein or its branches, or upon the gall ducts, and thus 
seriously interfere with the functions of the organ. Sometimes, how- 
ever, the tumors are very large and abundant without causing any 
apparent detriment to the liver functions. They are not infrequently 
stained with bile. Melanotic carcinomata sometimes occur in the 
liver, most frequently as secondary tumors. 

In some cases, instead of forming separate, distinct nodules, the 
cancerous growth develops in the form of a diffuse infiltration of the 
organ, so that the often greatly enlarged liver is irregularly mottled 
with white and reddish-brown masses, and may then somewhat 
resemble some forms of chronic interstitial hepatitis. 

Sarcomata. — Spindle-celled, melanotic, and telangiectatic sarco- 
mata may occur in the liver as secondary tumors. Secondary nu/.vo- 
mata and cliondromata have also been described, but they are very 
rare. 

Cavernous lijmpliangiomata have been described in a few cases. 
Cysts, usually of small size, may occur by dilatation of the bile ducts. 
They may be multiple and contain serum, mucus, and degenerated 
epithelium. Single cysts, apparently unconnected with the gall ducts, 
are occasionally found in the connective tissue of the liver. They 
may be lined with ciliated epithelium. 

The liver is sometimes the seat of larger and smaller multiple 
cysts, varying from microscopical size up to that of a }>oa, and some- 



512 THE LITER. 

times larger. They do not appear to communicate with the gall ducts. 
They are sometimes associated with multiple cysts of the kidney. 
Their origin and nature are not understood. ^ 

Occasionally the liver is found at the autopsy, even if this be 
made but a few hours after death, more or less completely riddled 
Tvith small, irregular-shaped cavities, from the size of a pin^s head to 
that of a pea. These holes appear to be due to the accumulation of 
putrefactive gases in the liver, and close about them, as well as in 
the blood vessels, large bacilli and other forms of bacteria may be 
found. ^ 

PARASITES. 

Echinococcus. — This parasite is the most common and impor- 
tant of those which occur in the human liver. It forms the so-called 
hydatids of the liver. These represent one of the developmental 
stages of the small tapeworm of the dog, Tcenia echinococcus 
(see page 108). The cysts in the liver may be very small and multi- 
ple, but they may be as large as a man's head or larger. The liver 
may be greatly increased in size, and the tissue about the cysts 
atrophied. The liver itself furnishes a connective-tissue capsule, 
within which is the translucent, lamellated membrane furnished by 
the parasite. On the inside of this we may find a layer of cells, 
-granular matter, and a vascular and muscular system belonging to 
the parasite. Projecting from this inner capsule are the brood cap- 
sules and heads or scolices of the immature tapeworm. The sco- 
lices may become detached from the wall and lie free in the cavity, 
which is filled with a transparent or turbid fluid. 'Not infrequently 
the cysts are sterile, and are then simply filled with clear or turbid 
iiuid ; or the embryos may have died and disintegrated, and their 
detritus, including the booklets, may be intermingled with the fluid 
•contents of the cysts. The contents of the cysts may be mixed with 
fat, cholesterin crystals, pus, bile, or blood; or form a grumous 
.mass, in which we may or may not be able to find the booklets of 
the scolices or fragments of the lamellated wall. The connective 
tissue of the walls of the cysts may be greatly thickened, or they 
may be calcified. 

In other countries the lesion is much more common and fre- 
quently more formidable than in the United States. The cysts 
reach an enormous size, the veins of the liver may be compressed 



^ Consult Pye-Smith, " Cystic Disease of Liver and both Kidneys," Trans. London 
Path. Soc, vol. xxxii., p. 112, 1881. 

'"^ Freeman, Trans. New York Path. Society, 1889. Welch and Nuttall, Bull, of 
the Johns Hopkins Hospital, July-August, 1892. 



THE LIVER. 513^ 

and filled with thrombi, the bile ducts compressed and ulcerated. 
So much of the liver tissue may be replaced by the hydatids that 
the patient may die from this cause alone. Very frequently there is 
local peritonitis, and adhesions are formed between the liver and the 
surrounding parts. In some cases the cysts rupture, and their con- 
tents are emptied into the peritoneal cavity, the stomach, the intes- 
tines, the pleural cavity, or the lung tissue. Sometimes the cysts 
perforate the bile ducts, the vena cava, or some of the branches of 
the portal or hepatic veins. Sometimes the abdominal wall is per- 
forated and a fistula formed between the cavity in the liver and the 
surface. 

In cases in which we do not find the scolices entire, a careful ex- 
amination of the inner cyst wall or of its contents will frequently 
establish the diagnosis by revealing single booklets (see Fig. 35, page 
109) or fragments of the characteristically lamellated wall (see Fig. 
33, page 108). 

JEchinococcus muUilocularis, which is apparently an abortive 
form of the above species (see page 110), is very rare indeed in the 
United States. The writer (T. M. P.) has examined a specimen 
sent to him by Dr. Edward J. Ill, of I^ewark, IST. J., and which is 
now in the museum of the College of Physicians and Surgeons, 
New York. The patient was a male, age thirty-one, German, sin- 
gle, farmer. He had been in the United States five years. For a 
year previous to his death he had been out of health, and jaundiced 
and somewhat emaciated. A large, indistinctly fluctuating tumor 
was evident in the right lumbar and umbilical regions, and appa- 
rently connected with the liver. Aspiration of the tumor gave a 
milky fluid believed to be pus. An opening was made into the tu- 
mor by one of the surgeons attending the case, and death occurred, 
after ten hours, from hsemorrhage. 

The liver was found adherent to the abdominal walls, and about 
one-fourth of the right lobe of the liver was occupied by an irregu- 
lar cavity with very rough, ragged walls. These walls wore in 
some places from one to two inches in thickness, and appeared to 
the naked eye to consist of dense connective tissue in irregular 
bands and fascicles, which enclosed very irregular, mostly small 
cavities. Microscopical examination showed that the ca^-ities wore 
lined with the delicate, lamellated cuticula characteristic of the eohi- 
nococcus cysts. No booklets were found. Fig. 248 is a drawing 
from this specimen. 

Dtsfonia hepaticiim, D. sinense, D. Ja)iccoJaffH)K may occur in 
the gall ducts and gall bladder. D. sinense occurs especially in the 
East, and has been found in great numbers in the bodies of Cliina- 



514 



THE LIVER. 



men. D. hcematobium is very common in Egypt and Abyssinia, 
occurring in the blood vessels of the liver. 

Pentastoma deiiticulatum is the undeveloped form of Penta- 
stoiria taenioides, a parasite which inhabits the nasal cavity of dogs 
and some other animals. In the liver of man it usually occurs in 
the form of small, rounded, calcified cysts. The cysts may contain 
fat, calcareous matter, and the remains of the dead parasite, among 
which the booklets may be found. 

Ascaris Zu??i6?"icoi'des sometimes finds its way from the intestines 
into the bile ducts. It may cause no disturbance here, but in some 
cases the worms have been present in large numbers and caused 




Fig. 348.— Echinococcus MULTrLocuLAKis of the Livee, 

occlusion, dilatation, and ulceration of the biliary passages, and have 
led to the formation of abscess of the liver. 

Psorospermia, the very common parasite in the rabbit^s liver, 
has been found a few times in the liver of man. 



THE BILIARY PASSAGES. 

Catarrhal Inflammation most frequently attacks the lower por- 
tion of the common duct and the gall bladder. In the acute form 
it usually leaves but few changes appreciable after death. An ab- 
normal coating of mucus, and sometimes congestion of the blood 
vessels, are almost the only post-mortem lesions. Owing to the 



THE LIVER. olo 

;swelling of the mucous membrane and the accumulation of mucus in 
the himen, the ducts may be temporarily occluded, but this occlu- 
sion may not be evident after death. If, however, the inflammation 
becomes chronic, the walls of the bile ducts may become thickened 
and their lumina more or less permanently obstructed. In conse- 
quence of this, dilatation or ulceration of the bile ducts may ensue. 
Temporary obstruction of the bile ducts may produce marked pig- 
mentation of the liver, owing to the accumulation of pigment gran- 
ules in the liver cells, particularly in the vicinity of the capsule of 
Glisson, and jaundice of the entire body. 

The gall bladder may be inflamed by itself or in connection with 
inflammation of the biliary passages. If the disease is chronic the 
wall of the bladder may be thickened ; polypoid growths may occur 
in the mucosa ; the duct may be occluded ; dilatation, ulceration, 
the formation of gall stones, calcification, and atrophy may ensue. 

Inflammation of the stomach and duodenum, hypersemia and in- 
flammation of the liver, concretions, and parasites are the usual 
causes of catarrhal inflammation of the biliary passages, but it may 
occur without these. 

Suppurative and Croupous Inflammation may attack the bili- 
ary passages and produce infiltration of pus in their walls and puru- 
lent fluid in their cavities ; or flakes and tubular casts of fibrin on 
their walls ; or infiltration of their walls with fibrin, and consequent 
ulceration. These lesions occur most frequently in connection with 
obstruction of the bile ducts and in typhoid and typhus fever, pyae- 
mia, cholera, or they may be due to the extension of infiammatory 
processes from without. They also occur under unknoAvn condi- 
tions. Suppurative inflammation may produce perforations of the 
ducts or bladder, with escape of bile and peritonitis ; or fistulous 
openings between the gall bladder and the duodenum, colon, and 
stomach, or through the abdominal wall. Or the inflammation may 
extend to the liver tissue and produce abscesses. Under the latter 
conditions we may find a series of small abscesses ranged along the 
walls of the suppurating gall ducts. In more advanced stages the 
abscesses may become large and communicate with one another, so 
that a considerable portion of the liver may be occupied by a series 
of communicating cavities with ragged walls, containing pus and 
detritus of liver tissue more or less tiuii-ed with bile. 

These abscesses are apt to contain various forms of bacteria, but 
whether they always or frequently stand in a causative relation to 
the lesion or not has not been definitely estabhshed. 

Such abscesses may become more or less completely enclosed by 
oomiective-tissue walls. The portal vein may also become intiamed. 
mid perforations may be fc>i*7nivl bi^twtMMi it ami tlie bile ducts. 



516 THE LIVER. 

Constrictions of the biliary passages raay also be produced by the 
same causes. 

Constriction and Occlusion may be produced by inflammation 
of the ducts themselves, by new growths in their walls, by calculi or 
parasites in their lumina, by changes in the hepatic tissue in chronic 
and acute hepatitis, by aneurisms, or by pressure on the duct from 
without, as by tumors in the head of the pancreas, etc. 

The obliteration of the smaller bile ducts produces no marked 
lesions. When the ductus communis or the hepatic duct is ob- 
structed, the ducts throughout the liver are frequently dilated and 
the liver tissue bile-stained. The liver may undergo atrophy and 
the whole body be intensely jaundiced. When the cystic duct is ob- 
structed the gall bladder is dilatedo 

Dilatation of the bile ducts is usually produced by strictures in 
the ways just mentioned, or by calculi. When calculi have pro- 
duced the dilatation this condition may sometimes continue after 
they have found their way into the intestines. Sometimes, however, 
we meet with very marked dilatation of the bile ducts without being 
able to make out any present or past obstruction. The dilatation. 
may affect only the common and hepatic ducts, or it raay extend to 
the smaller ducts in the liver, which are then dilated uniformly or 
sacculated. They may contain bile, mucus, or calculi. The liver is 
at first enlarged, but may afterward atrophy. The gall bladder may 
be dilated in consequence of obstruction of the common or the cystic 
duct. In the latter case it may reach an immense size and form a 
large tumor in the abdominal cavityo The dilatation is generalljr 
uniform, the bladder retaining its normal shape ; sometimes, how-^ 
ever, there are diverticula, which are usually produced by calculi. 
If the obstruction to the hepatic duct is incomplete or movable the 
gall bladder may contain bile, and often calculi. If the obstruction 
is complete the contained fluid may gradually lose its biliary char- 
acter and become a serous or mucous fluid of a light-yellow color — 
hydrops cystidis felloe. The walls of the bladder may be of nor- 
mal thickness, or thinned, or thickened, or calcified. If the obstruc- 
tion is due to a calculus, this may pass into the intestine and the galL 
bladder be suddenly emptied. Usually the bladder fills again, owing 
to its loss of contractile power. 

Biliary Calculi. — These bodies are of common occurrence. Thej^ 
are found usually in the gall bladder, sometimes in the hepatic, 
cystic, and common ducts ; less frequently in the small ducts of the 
liver. In the gall bladder from 1 to 7, 800 calculi have been counted. 
They vary in size from that of a pin^s head to that of a hen^s Q^g, or- 
they may be larger. Single gall stones are usually spheroidal or ovoid- 
al ; when multiple they are usually flattened at the sides or faceted* 



THE LIVEK. 517 

They may be composed : 

1. Principally of cholesterin, and may be of pure white color, or 
tinged with various shades of yellow or brown by bile pigment. The 
fractured surface shows a radiating crystalline structure. 

2. Of cholesterin, bile pigment, and salts of calcium and 
magnesium. These are usually dark-colored, brown, reddish-black, 
or green, and may be spheroidal or faceted, smooth or rough on the 
surface ; the fractured surface is usually radiating crystalline. This 
is the most common form. 

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Fig, 249.— Primary Carcinoma of the Common Bile Dfct, x 300 and reduced. 

3. Principally of hile pigment. Such calculi are raro. usually 
small, very dark-colored, and not numerous. 

4. Of calcium carbonate. These are rare, have a nodular surfa('t\ 
and a clear crystalline, not radiating fracture. 

Most calculi are formed around a central mass, sometin\os called 
the nucleus, which may consist of cholesterin, bilo pigment, nuicus. 
or epithelium, or more rarely of some foreign body. Thus a do;ul 
parasite, a needle, and fruit seeds may servo as nuclei. The body of 
the calculus may be homogeneous, or laniellatod, or crystalline. 

Biliary calculi in the gall bladder may produce no symptoms anil 
only be discovered after death. In the hepatic and connnon duct > 
45 



518 THE LIVER. 

they may obstruct the flow of bile and produce fatal jaundice ; or 
they may pass from time to time into the intestine, producing biliary 
colic. If they are impacted in the cystic duct they may produce dila- 
tation of the gall bladder. They may get into the duodenum by 
ulceration through the walls of the ducts or gall bladder, or in the 
same way into the peritoneal cavity. Gall stones which get into the 
intestinal cavity usually pass off without doing any further injury, 
but very large calculi may cause occlusion of the gut with fatal 
results. 

TUMORS OF THE GALL BLADDER AND LARGER GALL DUCTS. 

Small fibromata have been described in the gall bladder and in 
the common duct, but they are very rare. The most common tumors 
are carcinomata. These may be primary or secondary, and present 
the usual structural variations. The cells may be cylindrical, poly- 
hedral, or they may present the characteristics of colloid cancer. 
Primary carcinomata of the gall bladder and larger ducts (Fig. 249) 
are not uncommon. N^ot infrequently the pancreatic and common 
ducts are both involved, and it is difficult to say whether the tumor 
is primary in the head of the pancreas or in the gall duct. The 
bladder and ducts may also be secondarily involved m carcinomata 
of the stomach, liver, and duodenum. 



THE SPLEEK 



In studying the alterations produced in. the spleen in disease it is 
important to bear in mind the peculiar relations in which this organ 
stands to the blood vessels and to the circulation. After passing 
through the various branches of the splenic artery and the limited 
systems of capillaries which are associated with it, the blood is not 
received at once into venous trunks, as in other parts of the body, 
but is poured directly into the pulp tissue. In this it circulates, un- 
der conditions which render it liable to stagnation and undue accu- 
mulation, before it is taken again into well-defined vessels through 
the open walls of the cavernous veins. Moreover, these conditions 
naturally unfavorable to undisturbed and vigorous circulation, are 
reinforced by the association of the splenic with the sluggish and 
often interrupted portal circulation. Bearing these considerations in 
mind, it will be in a measure plain why, as is in fact the case, the 
spleen should be more liable to alterations in size than any other or- 
gan in the body, and why, serving as it does as a sort of blood filter, 
it should be especially susceptible to the influence of deleterious ma- 
terials of various kinds which in one way or another gain access to 
the blood. In this respect the relations of the spleen to the bkx^d, 
and of the lymph nodes to the lymph, present suggestive analogies. 

WOUNDS, RUPTURE, AND HAEMORRHAGE. 

Wounds of the spleen are usually accompanied by extensive 
haemorrhage and are commonly fatal. Death usually occurs as the 
result of this liiBmorrhage, but it may be due to secondary inriam- 
matory changes. Healing and recovery may, however, occur. 

Ruptttre of the spleen may be traumatic or spontaneous. In the 
former case it may be due to direct violence in the region of the or- 
gan or to injury to the thorax, falls, etc. In certain diseased condi- 
tions the spleen is more liable to rupture than when it is normal. 
Tlie rupture usually involves not only the capsule, but a more or 
less considerable portion of the parenchyma, and of course leads to 



5,20 



THE SPLEEX. 



hemorrhage. Spontaneous rupture is rare, but may occur as the 
result of excessive enlargement of the organ, as in typhoid fever, 
malaria, etc. — see below — or as the result of abscess. 

Hcemorrhage. — Aside from the extensive haemorrhages from in- 
jury and rupture, the spleen may be the seat of small circumscribed 
hemorrhages in various infectious diseases, although, omng to the 
peculiar distribution of the blood, it is often very difficult to distin- 
guish between a moderate interstitial hemorrhage and hyperemia. 

DISTURBAXCES OF THE CIRCULATION. 

Ancemia. — This may be associated Avith general anaemia, but it 
is not always present in this condition When marked and unasso- 




Fig. 250. — Congestion of the Spleen. 

b, dilated cavernous veins; c, trabeculae of pulp tissue compressed between dilated cavernous 
veins; c7, glomerulus. 



ciated with other lesions the spleen is apt to be diminished in size, 
the capsule more or less WT.'inkled, the cut surface dry and lighter 
in color than normal, the trabecule unduly prominent. 

In this, as in other alterations simply of the blood content of the 
spleen, neither the gross nor microscopical appearances are constant, 
because of the redistribution of blood which is apt to occur in the 
"^'iscera after death. 

Hypercemia. — This may be passive, occurring when some ob- 
struction to the portal circulation exists, most frequently in cirrho- 
sis of the liver, but also with certain valvular lesions of the heart, 
emphysema, etc. The spleen is enlarged, but usually only to a 
moderate degree. The capsule is apt to be tense, and on section the 



THE SPLEKX. 521 

pulp is dark-red and may be soft or firm. The cavernous veins are 
dilated (see Fig. 250). Usually, when the lesion has existed for 
some time, there is a thickening of the trabeculsB and reticular 
framework of the spleen, so that they are prominent on section. In 
other words, there is a chronic interstitial splenitis following the^ 
chronic congestion. 

Active Congestion of the spleen, which in most cases is scarcely 
to be differentiated from some forms of acute inflammation, and 
probably in many cases is associated with it, very frequently occurs 
in a great variety of acute and infectious diseases, such as typhoid 
fever, pneumonia, diphtheria, pysemia, the exanthemata, etc. The 
spleen is enlarged, the capsule tense ; on section the pulp is soft, 
dark-red in color, often swelling out from the cut surface and con- 
cealing the glomeruli and trabeculse. Under these conditions we 
may find the cavernous veins distended with blood and the inter- 
stices of the pulp infiltrated with a variable, sometimes large quan- 
tity of red and white blood cells. Or we may find, in addition to this. 
an increase in cells, which characterizes acute inflammation or hy- 
perplasia of the spleen (see below). 

Infarctions of the Spleen. — Embolic infarctions of the spleen 
are of frequent occurrence. They may be single or multij^le, small 
or very large, sometimes occupying half of the organ. They are in 
general approximately wedge-shaped, corresponding to the area of 
tissue supplied by the occluded artery. They may be hsemorrhagic. 
i.e., red, or they may be white (see page 62). Infarctions, originally 
red, may become white after a time from changes in the blood pig- 
ment. They may usually be seen as dark-red, reddish- white, or 
white, hard, sometimes slightly projecting areas on the surface of tlie 
organ. IN^ot infrequently the centre of the infarction is light in color, 
while the peripheral zone is dark-red. A layer of fresh fibrin is 
sometimes seen over the surface of the infarction. The general as 
Avell as the microscopical appearances which they present depend 
largely upon the age of the infarction. In the earlier stages the 
luBinorrhagic infarctions present little more under the microscope 
than a compact mass of red blood cells, among which may be seen 
the compressed necrotic parenchyma. The white infarction may 
show at first in a general way the usual splenic structure, but the 
entire tissue is in a condition of coagulation necrosis. The tissue 
may disintegrate and soften, and be more or less completely ab- 
sorbed, with or without fatty degeneration. A zone of inflamma- 
tory tissue ma}" appear around the infarction and upon the capsule, 
and this tissue, becoming denser, assumes the characters of cicatri- 
cial tissue and contracts around the unabsorbed remnant of the in- 
farction, so that finallv nothing' mav be left but ;i dense mass of 



622 THE SPLEEN. 

fibrous tissue, which frequently draws in the surface, causing more 
or less distortion of the organ. This cicatrix may be pigmented or 
white. 

If the embolus be of an infectious, irritating nature, in addition 
to its mechanical effects there may be suppuration, gangrene, and 
the formation of abscess. There may be perforation of the capsule 
and fatal peritonitis. 

INFLAMMATION. 

Acute Hyperplastic Splenitis (Acute Splenic Tumor). — The 
conditions under which acute inflammation of the spleen occurs 
have already been mentioned under active hypersemia, with which 
it is usually associated. It is a frequent though not a constant ac- 
companiment of the acute infectious diseases, and seems in all cases 
to be a secondary lesion. The spleen is enlarged, sometimes to two 
or three times its normal size. On section the pulp is soft, often 
almost diffluent, and projects upon the cut surface. The color is 
sometimes dark-red, sometimes grayish-red, or mottled red and gray. 
The trabeculae and glomeruli are usually concealed by the swollen 
and softened pulp, but the glomeruli are sometimes unusually promi- 
nent. 

Microscopical examination shows the marked increase in size to 
be due in part to the hyperaemia; in part to a swelling and increase 
in the number of cells, sometimes of the pulp, sometimes of the 
glomeruli, or of both. We find large, multinucleated cells ; cells 
resembhng the ovoidal and polyhedral cells of the pulp, but larger 
and with evident division of the nuclei. Cells resembling leuco- 
C3"tes may be present in large numbers, and larger and smaller cells 
in a condition of fatty degeneration, or containing pigment, are 
often seen. The elongated cells lining the cavernous veins may be 
swollen or increased in number. IRot infrequently larger and 
smaller cells are found which contain structures looking like red 
blood cells or their fragments. In some cases, particularly in scar- 
latina, hyperplasia of the glomeruli is a prominent feature. In some 
oases, particularly in typhus and recurrent fevers, the cells of the 
glomeruli undergo marked degenerative changes, so that they may 
form small softened areas looking like little abscesses. Small ne- 
crotic areas, often associated \vith localized suppuration, are some- 
times found in typhus and typhoid fever, scarlatina, etc. , and may 
be due to infectious emboli. As the primary disease runs its course 
the swelling of the spleen subsides, the capsule appears wrinkled, 
the color becomes lighter, and sometimes the organ remains for a 
long time, or permanently, small and soft. 

The cause of these marked changes in the spleen in infectious 
diseases is not understood. It seems probable that they are due to 



THE SPLEEN. 523 

the lodgment in the organ of some deleterious materials which have 
found access to the blood. Whether these materials are bacteria, or 
products of the life processes of bacteria, or something entirely 
apart from these, we do not in many cases know. Bacteria have, 
indeed, in many cases been found in the organ under these condi- 
tions, but by no means with the frequency and abundance which tlif* 
commonness and prominence of the lesion would lead us to expect 
if it were in all cases due to their presence. 

Suppurative Splenitis (Splenic Abscess). — Small abscesses may 
be found in the spleen as the result of minute infectious em^boli, and 
these may coalesce to form larger abscesses ; but larger and smaller 
abscesses may form in the spleen without evidence of their embolic 
origin. Sometimes the entire parenchyma is converted into a soft, 
necrotic, purulent mass surrounded by the capusle. It is rare for 
simple infarctions to result in abscess, but it does occasionally occur. 
Abscess of the spleen may occur from the propagation of a suppu- 
rative inflammation to the organ from adjacent parts ; from peri- 
nephritic abscesses, ulcer and carcinoma of the stomach, etc. Ab- 
scesses of the spleen may open into the peritoneal cavity, inducing 
fatal peritonitis, or, owing to an adhesive inflammation, the opening- 
may occur into the post-peritoneal tissue, into the pleural cavity, 
lung, stomach, intestines, or it may open on the surface. On the 
other hand, the contents of the abscess may dry, shrink, and be- 
come encapsulated and calcified. Abscesses may occur in ulcera- 
tive endocarditis, pysemia, typhoid fever, and more rarely in inter- 
mittent fever, and under a variety of other conditions whose nature 
is unknown to us. 

Chronic Indurative Splenitis (Chronic Splenic Tumor). — There 
may be, as we have already seen, a new formation of connective 
tissue in the spleen as a result of chronic congestion or infarctions, 
or about abscesses. But there is a more diffuse formation of con- 
nective tissue, usually in the nature of an hyperplasia, which oc- 
curs under a variety of conditions, and is now marked and exten- 
sive, and again comparatively ill-defined. It is always associated 
with more or less extensive changes in the parenchyma. In its 
most marked form it is found in chronic malarial pivlsoning, and 
under these conditions it may be found not only in persons who have 
suffered from repeated attacks of intermittent fever, but also in those 
who have not thus suffered but have resided in malarial regions. 
The enlarged spleen is often called ** ague cake." Similar condi- 
tions, though usually less marked, may occur in congenital and ac- 
quired syphilis, from prolonged typhoid fm-er, and as a result of 
acute hyperplastic splenitis from various causes, and also in leukannia 
and pseudo-leuktBmia. 



o'U 



THE SPLEEX. 



The gross appearance of the spleen in chronic indurative splenitis 
varies greatly, both in the size of the organ and in the appearance of 
the section. The spleen may be enormously enlarged or it may be 
of about normal size. It is usually, however, enlarged. The cap- 




Fig. 251.— Chronic Indurative Splenitis. 
Sho-wing s-vvelling or proliferation of the lining cells of the cavernous veins. 

sule is usually more or less thickened, frequently unevenly so. The 
consistence is usually considerably increased, but this is not always 
the case. The color and appearance of the cut surface present 










Fig. 252.— Chronic Interstitial Splenitis. 
a. thickened capsule: 6, thickened trabeculse; c. dilated cavernous veins; d, dense pulp tissue 
with obliterated cavernous veins. 



much variation. It may be nearly normal or it may be grayish, or 
dark-brown, or nearly black. The color may be uniform or the sur- 
face may be mottled. The glomeruli may be scarcely ^^isible or 



THE SPLEEN. 



r,2o 



very prominent ; the trabeculse are in some cases nearly concealed by 
the pulp ; in others they are large, prominent, and abundant, so that 
the surface is crossed in all directions by an interlacing network of 
broader and narrower irregular bands, between which the red or 
brown or blackish pulp lies. 

Not less varied are the microscopical appearances of the spleen 
under these conditions. In one class of cases there is more or less 
uniform hyperplasia of both pulp and interstitial tissue. The paren- 
chyma cells are increased in size and number ; there may be swell- 
ing and proliferation of the lining cells of the cavernous veins (see 
Fig. 251). The reticulum of the pulp, as well as that of the glome- 
ruli, and also the trabeculse, are thickened. In another class of 
cases the thickening of the reticular and trabecular tissue, either uni- 
formly or in patches, is the prominent feature (Fig. 252), while the 
changes in the pulp are rather secondary and atrophic. In both 
forms irregular pigmentation is frequent, the pigment particles being 




Fig. 253.— Malarial Spleen. 
Showing thickening of the trabecular network of the pulp, with pigmentation of the pulp cells. 



deposited either in the cells of the pulp or glomeruli, or in the new- 
formed interstitial tissue (Fig. 253). Finally, there are all interme- 
diate forms of induration between those described, and the changes 
are by no means uniform in the same organ. When these spleens 
are large they are liable to displacement. 

Syphilitic Splenitis. — This lesion may present itself as an in- 
durative process due to the formation of new connective tissue, and 
present no distinct morphological characteristics. In rare cases, 
however, gummata may be present in connection with the new 
fibrous tissue ; then the nature of the lesion becomes evident. 

Tubercidar Splenitis. — This lesion is secondary, either to tuber- 
cular inflammation in some other part of the body, or is the result of 
the general infection in acute general miliary tuberculosis. The tuln^r- 
cles may be very numerous and still invisible to the naked eye, or thoy 
may be just visible, or as large as a pin's head or thereabouts, and 
very thickly strewn through the organ or sparsely scattereil . In otiier 
4G 



526 THE SPLEEN. 

cases the tubercles are larger, sometimes as large as a pea, and they 
are then usually not very numerous. Microscopically they present the 
usual variety of structure, sometimes as simple tubercle granula, 
sometimes as conglomerate tubercles ; they may consist simply of a 
collection of small spheroidal cells, or there may be larger polyhedral 
cells and giant cells with a well-defined reticulum. Cheesy degene- 
ration occurs under the usual conditions. Tubercle bacilli a.re usu- 
ally present, particularly in the more acute forms, sometimes in 
small, sometimes in enormous numbers. They seem to be especially 
abundant in acute general miliary tuberculosis of children. These 
tubercles may be formed in the glomeruli, in the walls of the smaller 
arteries, in the pulp tissue, and in the trabeculse and capsule. Owing 
to the peculiar character of the spleen tissue the earlier stages are 
not readily recognized, since simple collections of small spheroidal 
cells are not distinctly outlined against the normal tissue. There is 
frequently a moderate swelling of the spleen, owing to hypersemia 
and hyperplasia of the parenchyma. 

Perisplenitis. — Acute inflammation of the capsule of the spleen 
may occur as a part of a general or localized peritonitis, or as a re- 
sult of lesions of the spleen itself, such as infarctions, abscesses, and 
acute hyperplastic inflammation. Under these conditions a fibrinous 
pellicle, with more or less pus, may be formed on the surface of the 
organ. Chronic pejnsplenitis, resulting in the production of new 
connective tissue, either in patches or as a more or less general thick- 
ening of the capsule, is of frequent occurrence. It may follow acute 
inflammation of the capsule, or be a part of general or localized 
chronic peritonitis. It is common in connection with chronic indura- 
tive splenitis, and it may occur from unknown causes. Sometimes 
the capsule is three or four mm. in thickness over a considerable 
area ; sometimes very small nodular thickenings or papillary projec- 
tions occur. As a result of this process adhesions, sometimes very 
extensive, may form between the spleen and adjacent parts. The 
thickened capsule is sometimes more or less extensively calcified. 

Alterations of the Spleen in Leukcemia and Pseudo-LeukcEmia. 
— The lesions of the spleen are essentially the same under both of 
these conditions. They consist, in general, of an hyperplasia, some- 
times most marked in one, sometimes in another of the structural 
elements of the organ, but usually they all participate in the altera- 
tions. The changes which occur in the earlier stages are but little 
known. The gross appearances of the spleen, as we find them in 
persons dying of either of the above diseases, present considerable 
variation. They are usually enlarged and sometimes are ten or 
fifteen times the normal size. They are usually hard, but are some- 
times of the ordinary consistence, or softer. The capsule is usually 



THE SPLEEN. 627 

thickened and rough. The section of the spleen may be of a uniform 
dark-red color, but it is more frequently mottled red and gray. 
Sometimes the glomeruli are inconspicuous, but they are very often 
enlarged and prominent. They may be two to four mm. in diameter, 
and, owing to an infiltration of the arterial sheaths with lymph cells, 
may appear to the naked eye as grayish, round or elongated bodies, 
arranged along branching, interrupted, grayish streaks. The trabe- 
cula may be greatly thickened, as also the reticulum of the pulp, so 
as to be evident to the naked eye. Brown or black pigment may be 
collected around the glomeruli or in the pulp. Hsemorrhagic infarc- 
tions or circumscribed extravasations of blood may further compli- 
cate the picture. 

Microscopically the appearances are essentially the same as those 
above described in acute hyperplasia and in chronic interstitial sple- 
nitis, depending upon the stage and variety of the disease. Owing 
to the great size which some of these spleens attain they are liable to 
displacement, and they may interfere by pressure with the functions 
of neighboring organs. 

DEGENERATIVE CHANGES IN THE SPLEEN. 

Atrophy. — The spleen may become atrophied in old age ; as a 
result of prolonged cachexige, and in connection Avith profound and 
persistent anaemia ; or, more rarely, from unknown causes. The 
capsule may be wrinkled and thickened, the color pale, the trabecula 
prominent, the consistence increased. The change is largely in the 
pulp, whose parenchyma cells are decreased in number. 

Amyloid Degeneration. — This degeneration may affect the glo- 
meruli or the pulp tissue, or both together. When confined to the 
glomeruli the spleen may or may not be enlarged, and the cut sur- 
face is more or less abundantly sprinkled with round or elongated, 
translucent bodies resembling considerably in general appearance 
the grains of boiled sago. These are the waxy glomeruli. Such 
spleens are often called ''sago spleens ^^ (Fig. 254:). Microscopical 
examination shows that the degeneration is confined to the walls of 
the arteries, capillaries, and reticulum of the glomeruli, withatropliy 
and disappearance of the lymphoid cells. 

In other cases, either with or without involvement of the glo- 
meruli, there is waxy degeneration of the bloml vessels and reticu- 
lum of the pulp, which may occur in patches or bo general and 
more or less excessive. If the alteration is general and consider- 
able the spleen is enlarged, its edges rounded, its consistence in- 
creased. On section it appears translucent, and the distribution of 
the degenerated areas may be readily seen by holding a thin slice 
up to tlie liglit. The spleen may be alone atVected, or tliero may bv^ 



528 



THE SPLEEN. 



similar degenerations in other organs. The general conditions under 
which this lesion occurs, and the methods of staining and studying, 
are given on page 80. 

Pigmentation of the spleen may occur as the result of the de- 
composition of hsemoglobin in the organ under a great variety of 
conditions : thus after haemorrhagic infarctions, small multiple haem- 
orrhages, acute hyperplastic splenitis, etc. Or the pigment may 
be anthracotic and be brought to the organs from the lungs or 
bronchial glands (see page 85). Bile pigment may also be deposited 
in the spleen in jaundice. The pigment may lie in the walls of the 
smaller arteries, in the cells and reticulum of the pulp, or free in the 
latter tissue, or in the follicles. It is usually quite unevenly dis- 




FiG. 254.— Amyloid Degeneration of Glomeruli of the Spleen— "Sago Spleen.' 
The " waxy " portions are stained red. 



tributed. The pigment may be red, brown, or black. According 
to Weigert anthracotic pigment may be sometimes seen with the 
naked eye in the periphery of the glomeruli as dark crescents. 

Primary tumors of the spleen are rare. Small fibromata, sar- 
comata, and cavernous angiomata sometimes occur. Sarcomata 
and carcinomata may occur in the spleen secondarily either as me- 
tastatic tumors or by extension from some adjacent part, as the sto- 
mach. Dermoid cysts are described, but are rare. Other larger 
and smaller cysts, whose mode of origin is in most cases obscure, 
not infrequently occur. 

PARASITES. 

Pentastomum denticulatum is not infrequently found in the 
spleen, usually encapsulated and calcified. Cysticercus is rare. 



THE SPLEEN. 529 

Echinococcus is occasionally found, and, if t*he cysts are large or 
numerous, may cause more or less extensive atrophy of the organ. 

Various forms of bacteria have been found in the spleen. Micro- 
cocci have been found in pyaemia, small-pox, ulcerative endocar- 
ditis, diphtheria, and under other conditions. The Bacillus anthra- 
cis occurs here in anthrax ; the Bacillus tuberculosis in tubercular 
inflammation ; and bacilli have been described in typhoid fever. 
Spirochcete Obermeieri may be found in relapsing fever. 

MALFORMATIONS AND DISPLACEMENTS. 

The spleen may be absent in acephalous monsters, and with de- 
fective development of other abdominal viscera. Very rarely it is 
absent in persons who are otherwise perfectly developed. Small 
accessory spleens, from the size of a hazelnut to that of a Avalnut, 
are not infrequent. They usually lie close to the spleen, but may 
be considerably removed from it ; thus they have been found em- 
bedded in the head of the pancreas. Two spleens of about equal 
size have been observed. The form of the spleen is subject to con- 
siderable variation. It may be made up of several distinct lobes. 
It may be displaced congenitally or as the result of disease. It may 
be on the right side in transposition of the viscera. As the result 
of congenital defects in the diaphragm the spleen may be found in 
the thorax ; or in deficient closure of the abdominal wall it mav, 
together with other abdominal viscera, be found outside of the body. 

The spleen may be pressed downward by any increase in the con- 
tents of the thorax. It may be fastened by adhesions to the concave 
surface of the diaphragm,- so that its long axis is nearly horizontal 
instead of vertical. It may be displaced by changes in the contents 
of the abdominal cavity. If the organ is increased in size it fre- 
quently becomes tilted, so that its lower border reaches the right 
iliac region. If the ligaments are too long congenitally, or if they 
are lengthened by traction, and if the organ is at the same time in- 
creased in weight, it may become very movable. It may sink down- 
ward, with its hilus turned upward ; or it may be rotated on its axis, 
and, owing to torsion of the vessels thus produced, the organ may 
atroph}^ ; or the pressure of the ligaments and vessels across the 
duodenum may cause occlusion of the gut. 



THE PAXCBEA 






The diseases of the pancreas appear, so far as we know, with a 
few exceptions, to be of Httle practical importance ; that is, they do 
not often give rise to symptoms of disease or cause death, but the 
lesions are found in the bodies of persons dead from other diseases. 
It is probable, however, that in many cases their apparent insignifi- 
cance is due to our lack of knowledge of the interference with func- 
tions which lesions of the gland induce, and to the incomplete exami- 
nation of the pancreas which is so common at autopsies. 

Hcemorrliage into the substance of the pancreas may occur as the 
result of injury ; in the haemorrhagic diathesis ; in connection with 
valvular diseases of the heart or interference with the portal circula- 
tion ; or in connection with extensive fatty degeneration and fat 
necrosis of the' organ. Such hcBmorrhages may be minute or exten- 
sive. Several cases of sudden death are recorded in which the only 
discoverable lesion was an extensive haemorrhage into the substance 
of the gland and the tissue about it. In these cases it has been as- 
sumed that death was caused by interference with the hearths action, 
through pressure on the solar plexus and semilunar ganglion, but it 
may be due to other causes (see below. Fat !N"ecrosis). The haemor- 
rhage may be moderate and limited to the pancreas, or it may ex- 
tend into the subperitoneal tissue for a considerable distance. 

Haemorrhage of the pancreas may be associated with acute in- 
flammatory changes and with more or less extensive gangrene of 
the organ. The gangrenous pancreas may be more or less encapsu- 
lated ;* it may he, bathed in pus, in the abdominal cavity ; it may, 
by ulceration of the intestinal wall, get into the gut and be dis- 
charged ^vith other intestinal contents. 

INFLAMMATION. 

In some cases of typhoid fever, pyaemia, yellow fever, and other 
acute infectious diseases, the pancreas is red, swollen, and oedema- 
tous. Microscopically the most prominent lesion is a swelling and 



THE PANCREAS. 531 

undue granulation of the glandular epitlieiium, and hyperiemia. 
This condition is known as Parenchymatous Pancreatitis, 

SupjJtoratlve Pancreatitis is not very common, and may be 
primary or due to the extension of a suppurative inflammation from 
adjacent or distant parts of the body. There may be a diffuse infil- 
tration of the organ, with pus cells or larger and smaller abscesses. 
The abscesses may open into the gastro-intestinal canal or into the 
peritoneal cavity. The causes of primary suppurative pancreatitis 
are often most obscure. It may be associated with fat necrosis and 
with haemorrhage and gangrene of the pancreas. 

Chronic Interstitial Pancreatitis (Cirrhosis of the Pancreas). — 
This lesion consists in an increase of interstitial connective tissue, 
which may be general or confined to some particular portion of the 
gland. The organ is sometimes enlarged, sometimes smaller than 
normal. It is usually dense and hard ; secondary atrophy of the 
parenchyma regularly occurs. It may be due to chronic inflamma- 
tory processes in the vicinity of the organ. 

Syphilitic Inflammation. — Chronic interstitial pancreatitis is 
frequently found in congenital syphilis of the new-born, and the gross 
and microscopical lesions are similar to those above described. It is 
not definitely established whether or not a similar lesion may be 
caused by acquired syphilis. Gummata are very rare in the pan- 
creas, but have been described in congenital syphilis in very yoiuig 
children. 

Tubercular Inflammation. — Larger and smaller tubercles and 
tubercular, cheesy nodules are occasionally found in the pancreas in 
connection with acute general miliary tuberculosis or y^nih. tubercular 
inflammation in some other organ, particularly with that of adjacent 
lymph nodes, the lungs, and the intestine. 

DEGENERATIVE CHANGES IX THE PANCREAS. 

Atrophy of the pancreas may occur in old age and as a result of 
pressure from tumors or other adjacent structures. Marked atrophy 
of the pancreas is found in a certain proportion of cases of diabetes 
mellitus, but it is not constant. 

Fatty Degeneration of the parenchyma cells may occur, and in 
some cases is so extensive as to lead to nearly complete destruction 
of their protoplasm. 

Fatty Infiltration, which should be distinguished from fatty 
degeneration, consists in the accumidation of fat in the interstitial 
tissue of the ghmd. This may bo so excessive as to cause noarly 
entire destruction of the i>iand structures. Under these conditions 
the outline of the organ may be preserved, the fat being enclosed by 
the capsule. 



532 



THE PANCREAS, 



Amyloid Degeneration. — This usually occurs in connection with 
similar degeneration in other organs, and is confined to the walls of 
the blood vessels and the interstitial tissue. 

Fat Necrosis. — A very peculiar lesion of the fat tissue, most 
frequently seen in the fat tissue about the pancreas or between its 
lobules, but sometimes in fat tissue in other parts of the body, has 
been a few times described and called fat necrosis. White or yel- 
lowish nodules, varying from the size of a pin's head to that of a pea 
or larger, are seen embedded in the fat, the central portion being 
often soft and grumous and readily squeezed out. They are some- 
times calcified and sometimes surrounded by a connective-tissue 




Fig. 255.— Fat Necrosis in the Pancreas. 

Drawn from a specimen prepared by Dr. Ira Van Gieson and reported to the New York Patho- 
logical Society, 1888. 

capsule. Microscopical examination shows degeneration and dis- 
integration of the fat tissue (Fig. 255). They are most frequently 
found in marasma,tic persons. When the lesion is extensive, accord- 
ing to Balser, it may cause death, either directly or by inducing 
hsemorrhage. Some of the extensive haemorrhages about the pan- 
creas, above mentioned, may be caused in this way. ^ 

' For a detailed consideration of acute inflammation, haemorrhage, gangrene, and fat 
necrosis of the pancreas, with bibliography, consult FitZy Middleton Goldsmith lecture 
for 1889 on "Acute Pancreatitis," Transactions New York Pathological Society, 
1889. For special studies on fat necrosis consult Langerhaus, Virchow's Archiv, 
Bd. cxxii., p. 252, and in the " Festschrift " for Virchow's seventy-first birthday. 



J 



THE PANCREAS. 6'dk 

TUMORS. 

Carcinomata are the most common and important of the tumors 
of the pancreas. They may be primary or secondary. Primary 
carcinomata are most frequently found in the head of the organ, but 
may occur in other parts. The hard or scirrhous form is most com- 
mon, but occasionally soft and succulent and colloid forms are 
found. They are liable to involve adjacent parts by continuous 
growth, and may form metastases in the liver, adjacent lymph 
nodes, etc. Secondary carcinoma in the pancreas may occur in 
carcinoma of the stomach, duodenum, and the gall ducts and gall 
bladder. As a result of carcinoma of the pancreas, aside from the 
extension of the growth, there may be pressure on the ductus chole- 
dochus, with jaundice ; or on the pancreatic duct, with cystic dila- 
tation ; or pressure on the duodenum, with stenosis of the gut ; or 
pressure on the vena cava, or portal vein, or superior mesenteric 
vein, etc., with disturbances of the circulation. 

Concretions of carbonate and phosphate of lime are frequently 
found in the pancreatic ducts. They are usually multiple, small, 
whitish, smooth, or of rough and irregular shape. Sometimes, how- 
ever, they reach a diameter of more than an inch. They consist 
chiefly of calcium phosphate and carbonate. Besides these free con- 
cretions the walls of the ducts are sometimes encrusted with salts of 
lime. Such concretions may produce dilatation of the pancreatic 
ducts and large cysts, or more rarely abscesses. 

Foreign Bodies. — Gall stones sometimes find their way into the 
pancreatic duct. Ascarides have been found in the ducts in a con- 
siderable number of cases. 

Dilatation of the pancreatic ducts and the formation of cysts 
take place in several different ways. 

1. The entire duct may undergo a uniform cylindrical dilatation. 
With this cylindrical dilatation we sometimes find associated small 
sacculi. 

2. There may be sacculated dilatations at some point in the ducts. 
These dilatations form cysts of large size, as large even as a child's 
head. Their walls frequently undergo degeneration and calcifica- 
tion. These cysts often become filled with blood, and may then be 
mistaken for aneurisms. 

3. The small branches of the pancreatic duct may be dilated s^^ 
as to form a number of small cysts. These cysts are filled with 
serum, mucus, pus, or a thick, cheesy material. 

MALFORMATIONS AND DISPLACEMENTS. 

The pancreas may be entirely absent in aneucephalous and doubh^ 
monsters, and in congenital umbilical herniie. The pancreatic duct 

47 



534 THE PANCREAS. 

may be double ; it may open into the duodenum at some distance 
from the biliary duct, or into the stomach. The head of the pancreas 
may be unduly developed, and sometimes even completely separated 
from the rest of the organ, opening into the duodenum with a duct 
of its own. Occasionally there is a small accessory pancreas situated 
beneath the serosa of the duodenum or stomach. 

The pancreas is so firmly bound down that its position is not often 
changed. Sometimes, however, it is found pressed downward by 
tight lacing, displaced by aneurisms, or contained in umbilical and 
diaphragmatic hernise. 



THE SALIVARY GLA:^DS. 



THE PAROTID, SUBMAXILLARY, AND SUBLINGUAL. 

INFLAMMATION, 

This condition is most frequent and important in the parotid. 
The lesions of the epidemic disease known as mumps are most fre- 
quently confined to the parotid gland of one side, but the submaxil- 
lary and sublingual may be at the same time involved. The gland 
is swollen and there is often oedema of the mucous membrane of 
the mouth and pharynx. Very little is known of the actual minute 
changes which the gland undergoes in this disease. 

Acute parotiditis occasionally occurs as a secondary lesion in a 
variety of diseases, as in typhoid and scarlet fever, pysemia, pneu- 
monia, etc., and by propagation of inflammation from the mouth. 
Under these conditions the inflammation is usually suppurative and 
frequently results in abscess or sloughing. The interstitial tissue 
of the gland is more or less densely infiltrated with pus cells, and 
the parenchyma cells may undergo fatty degeneration and disin- 
tegration. The inflammation may be confined to the gland or it 
may spread to adjacent parts, sometimes causing much destruction 
of tissue, and may give rise to inflammation of the brain or of the 
inner ear, or even to metastatic pyaemic abscesses in different parts 
of the body. Healing may occur, with the formation of salivary 
fistuliB. 

The submaxillary gland may bo involved with the parotid in the 
suppurative inflammation. 

Acute suppurative inflammation of the connective tissue about 
the sahmaxillanj gland is sometimes of serious import. Sloughing 
and gangrene may occur and are apt to spread to adjacent parts. 
SepticjTBmia, oedema of the glottis, or pneumonia may coinpHoato the 
process and cause death. 

The sublingual gland is not often the seat of iuthnumation. 

CJiroiiic ill /lannudf ion, leadiui;' to tlie formation of dense inter- 



536 THE SALIVARY GLANDS. 

stitial tissue, sometimes occurs in the salivary glands. This may 
occur by itself or follow an acute inflammation. 

The Excretory Ducts of the salivary glands may become in- 
flamed from the presence of foreign bodies or of concretions formed 
in them. They may become occluded from the presence of cal- 
culi or as the result of inflammation, and may thus become widely 
dilated both in the main branches and in the finer ramifications. 
The dilatation of Wharton's duct to form larger and smaller cysts 
containing salivary fluid, sometimes gives rise to very large and 
troublesome tumors which constitute one of the forms of ranula. 

TUMORS. 

Fibromata are of occasional occurrence in the parotid. Chon- 
dromata, sarcomcdcc and flbro-sarcomata, and myxomata, or more 
frequently mixed tumors formed of varied combinations of these, are 
of frequent occurrence in the parotid and of occasional occurrence 
in the submaxillary gland. These complex or mixed tumors are of 
more frequent occurrence in these glands than in any other part of 
the body, except possibly the ovary. They are sometimes rendered 
still more complicated in structure' by a partially atypical glandular 
growth lending them an adenomatous character, and by the forma- 
tion of cysts. Or they may present in parts a distinctly carcinoma- 
tous character. 

Fibrosarcoma and melano- sarcoma have been described. Pri- 
mary carcinoma of these glands is very rare. 

A case of rhabdomyoma of the parotid gland, with evidences of 
atypical development of portions of the gland, has been described by 
one of us. ^ 

PARASITES. 

Echinococciis has been observed in the parotid gland. 

' Frudden, "Rhabdomyoma of the Parotid Gland," American Journal of the 
]Medical Sciences, xVpril, 1883. 



THE THYROID GLAIS'D. 



Hyperceinia of the thyroid gland, often accompanied by consid- 
erable enlargement of the organ, may be the result of valvular dis- 
Ipase of the heart ; it occurs in Basedow's disease ; it may be tem- 
porary or permanent, and in the latter case may give rise to the 
formation of new connective tissue. Haemorrhages may occur, 
causing pigmentation of the organ. 

Inflammation of the thyroid gland is not very common and 
may occur from a variety of causes. It may result in the formation 
of larger and smaller abscesses or in the production of new connec- 
tive tissue. Tubercular inflammation, with the formation of mih- 
ary tubercles, is of infrequent occurrence. Syphilitic inflamma- 
tion, with the formation of gummata, has been described, but is 
rare. 

Degeneration. — Colloid degeneration of the epithelial cells of 
the gland, and the filling of the alveoli with colloid material, is of 
common occurrence, and when occurring in moderate degree may 
be regarded as a normal event, since a certain amount of this 
change is found in many otherwise apparently normal glands. It 
may occur, however, to such an extent as to constitute a lesion (see 
below). 

Amyloid, degeneration, particularly of the blood vessels, is of 
infrequent occurrence. 

TUMORS. 

Among the most important of the lesions of the tln'roid is the 
enlargement of the organ commonly known as the goitre or struma. 
The enlargement of the gland may occur in several dilferent ways, 
and in only a part of the cases is to be considered as a tumor. 
Thus, a simple liypenBmia may, as above stated, cause considerable 
enlargement of the organ, and this is sometimes called .s^//7//y/(/ hy- 
percemica. The true goitre, however, consists in the enlargement 
of the old and the formation of new gland alveoli, while with these 
changes there is very frequently associated a greater or less amount 
of colloid degeneration. When there i^^ new formation o\' ulainl tis- 



538 



THE THYROID GLAND. 



sue the growth has the character of an adenoma. The hyperpla- 
sia may occur diffusely, so that the whole gland is more or less 
enlarged ; or it may occur in the form of circumscribed nodules. 
When the colloid degeneration is prominent, so that the tumor has a 
gelatinous look, it is called colloid struma (Fig. 256). Accumula- 
tions of fluid, blood, colloid, etc., in the old or new-formed alveoli, 
may cause dilatation and atrophy of the walls of the alveoli, so 
that cysts, sometimes of large size, are formed. Thus occurs the 
cystic struma. Again, the blood vessels may undergo marked dila- 
tation, so that we may have a telangiectatic struma ; or cavernous 
aiigiomata may form within them. Very frequently all these varie= 











w:^^MM: 








^1 %^;,..^€^m'fy^ 






Fig. 256.— Colloid Struma— Goitre. 
The colloid material filling the alveoli is stained red. 



ties of lesions are present in the same goitre. The appearances 
may be rendered still more complex by the occurrence of hsemor- 
rhages and pigmentation, calcification, purulent or indurative in- 
flammation, and by the not very infrequent association with carci- 
noma and sarcoma. The cause of goitre is not well understood. 
The growth is, as a rule, slow, but occasionally a very rapid ealarge- 
ment occurs as the result of a sudden increase of the colloid degene- 
ration. In many cases even very large goitres give rise to but 
moderate inconvenience, but they may assume great significance by 
encroaching upon neighboring parts. Thus death may be caused by 
pressure on the trachea, oesophagus, or on the large vessels. 



THE THYROID ULAXD. 530 

Sarcoma, either spheroidal or spindle-celled, may occur as primar}' 
tumors in the thyroid, either in otherwise normal glands or in con- 
nection with struma. Melano-sarcoma has been observed. Second- 
ary sarcomata are rare. 

Primary carcinoma, both glandular and scirrhous, occurs in the 
thyroid, and, particularly in the softer forms, may sj^read to adja- 
cent parts and occasionally form distant metastases. 

PARASITES. 

Echinococcus cysts have been found in the thyroid. 

MALFORMATIONS. 

The thyroid gland is sometimes very small, either as the result of 
atrophy or as a congenital deficiency. This is most marked in the 
condition called myxoedema (see below). 






W- 

M: 









Fig. 257.— Section of the Atrophied Thyroid Gland in Myxcedema. 

a, interstitial tissue; 6, atrophied lobules with small spheroidal-celled or lymphatic tissue in 
their peripheries. 

It may be irregularly lobulated. There may be small accessory 
glands situated at some distance from the normal position, as in the 
mediastinum or pleura. 

MYXCEDEMA. 

This disease occurs most frequently in middle-aged women, and 
its cause is unknown. The skin of the face is apt to be swollen and 
waxy, causing a peculiar and rather characteristic appearance of the 
features. The skin of the body is apt to be dry and rough, and tht^ 
hair may fall out. Perspiration is, as a rule, diminished. The men- 
tcil condition is dull, and loss of memory and insanity may cx'cur. 
Bodily movement and speech are apt to be impaired. 

The fat tissues may be atrophic, and the subcutanev)us tissue has 



540 THE THYROID GLAND. 

been shown in some, though not all, of the cases to contain an 
unusual amount of mucin. In some cases the fibres of the upper 
layers of the corium are crowded apart by fluid. 

The most marked and constant lesion in this disease is an atro- 
phic condition of the thyroid gland. The parenchyma of the gland 
is more or less completely replaced by fibrillar connective tissue and 
by new-formed reticular tissue resembling the lymphatic tissue of the 
lymph nodes. 

The general appearance of the atrophied thyroid gland is shown 
in Fig. 257. 

In a case .reported by Hun, which one of us has examined, the 
lobes of the thyroid measured less than one-half of an inch in dia- 
meter, and the entire gland weighed only about 7.2 gm. (112 grains). 

In addition to the lesion of the thyroid there are apt to be chronic 
endarteritis and chronic diffuse nephritis. In some cases there is 
an accumulation of small spheroidal cells about the smaller blood 
vessels in various parts of the body, and also petechial hsemorrhages- 

While the atrophy of the thyroid is the most marked and fre- 
quent lesion in this disease, our lack of knowledge about the function 
of this gland prevents a definite conception as to the relationship of 
this change to the symptoms. 

By the destruction of the thyroid from disease, or as the result of 
its removal in men and animals, a condition considerably resembling 
myxoedemals apt to be induced. 

Myxoedema appears to be identical with that condition which has 
been described as cachexia strumipriva. ^ 

THYMUS GLAND. 

Small accessory thymus glands are occasionally found near the 
thyroid. 

The thymus occasionally but not usually persists until youth or 
middle age instead of undergoing the usual developmental atrophy. 

Small hcemorrhages are described in the thymus of young chil- 
dren as the result of venous congestion in asphyxia, etc. They may 
also occur in the hsemorrhagic diathesis. 

Suppurative inflammation of the thymus is of occasional occur- 
rence, and is usually secondary to a similar inflammatory process in 
some other part of the body. 

Tubercular and syphilitic inflammation of the thymus are de- 
scribed. The sarcomata are the most common tumors of the thymus. 

^ For detailed descriptions of myxoedema, and the literature, see Hun and Prudden, 
"Myxoedema," Am, Jour. Med. Sciences, July and August, 1888, and " Report on 
Myxoedema" in Supplement to the Clinical Society Transactions, vol. xxi., London, 

1888. 



THE SUPEAEEI^AL CAPSULES. 



MALFORMATIONS. 

In acephalic and other monsters the suprarenal capsules may be 
atrophied or entirely absent. Sometimes in well-formed adults these 
organs cannot be discovered. 

There may be little rounded nodules loosely attached to the sur- 
face of the capsules and having the same structure. 

If one of the kidneys is absent or in an abnormal position its 
suprarenal capsule usually retains its proper position. 

HEMORRHAGE. 

In children, soon after birth, it is not very infrequent to find large 
haemorrhages in one of the capsules, converting it into a cyst filled 
with blood. The same lesion has been observed in a few cases in 
adults. 

THROMBOSIS, 

Klebs describes a case of capillary thrombosis of the cortex in 
both capsules iii a woman after excision of the knee joint. 

INFLAMMATION. 

Suppurative inflammation, with the formation of abscesses, has 
been seen in a few cases. 

The most frequent lesion of the suprarenal capsules is tubercular 
inflammation. They are usually increased in size, their surfaces 
are smooth or nodular. The normal structure of the gland is lost, 
and is replaced by tubercle tissue, connective tissue, and choosy mat- 
ter (see Addison's Disease). 

Syphilitic i)iflammation, with and without tho dovoh>i>nioiit of 
gummata, is of occasional occurrence. 

• 

DEGENERATION. 

Fattfi degeneration of the cortical portion o'i \\\c oapsulos is tho 
ruleiu the adult. It sometimes occurs in nodular areas. In children 
under five years of age it is a pathological condition. 

48 



54:2 THE SUPRARENAL CAPSULES. 

Amyloid degeneration may involve both the cortical and medul- 
lary portions. In the cortex it usually involves only the walls of 
the blood vessels ; in the medulla both the blood vessels and the 
cells of the parenchyma may undergo this degeneration. The cap- 
sules are usually firm and of a grayish, semi-translucent color. 

Pigmentation of the inner cortical zone is frequent in old persons. 

TUMORS. 

Carcinoma of the suprarenal capsules is not common. It may 
be primary, but is much more frequently secondary. Either one or 
both of the capsules may be the seat of the new growth. 

Sarcoma occurs as a primary and secondary growth. Probably 
many of the older cases described a.s cancers were really sarcomata. 

Cylindroma, — Klebs describes a growth of this character in one 
of the capsules, secondar}- to a tumor of the same kind in the supra- 
orbital region. He gives to such tumors the name of lymphangioma 
cavernosum. The exact character of these growths is still obscure. 
They consist of irregular follicles and cavities, lined with epithelium, 
and containing peculiar hyalin, structureless bodies. 

Cysts are found, both single and multiple. They are usually 
situated in the cortex. 

Neuroma. — Ganglionic neuromata have been described by Weich- 
selbaum^ and Freeman.' 

Glioma has been described as occurring in the medullary region. 

An hyperplasia of the gland tissue, \vith fatty degeneration in the 
form of circumscribed nodules, is described bv Virchow. 

' Weichselbaum, Yirch. Arcliiv, Bd. Ixxxv., p. 554. 

^ Freeman, Proceediags of the New York Pathological Society, 1893, p. 88. 



THE UBi:N"Ar.T APPARATUS. 



THE KIDNEYS. 



MALFORMATIONS. 



Entire absence of both kidneys is sometimes associated with great 
malformation of the entire body. Such foetuses are not viable. 

Absence of one kidney is not uncommon, the left kidney being- 
more frequently absent than the right. The absence of the kidney 
may be complete, the ureter being also absent ; there may be an ir- 
regular mass of much -atrophied kidney tissue with connective tissue 
and fat, or there may be only a little mass of connective tissue and 
fat representing the kidney, and a ureter running down to the blad- 
der. . The single kidney which is present is usually much enlarged. 
It may be in its natural position or displaced downward. 

Since the extirpation of the kidney has been practised by sur- 
geons it has been found that absence of one kidney is more common 
than was formerly believed. 

When both kidneys are present one of them may be much larger 
than the other. 

Sometimes one kidney will have two pelves or two ureters. 

A rather frequent malformation is the so-called horseshoe kidnef/. 
The lower ends of the kidneys are joined together by a commissure. 
The commissure is usually composed of kidney tissue, but some- 
times of connective tissue. The two kidneys may be normal, except 
for the commissure ; or their shape, the arrangement of the vessels 
and ureters, and the position, may be unnatural. 

The two kidneys may be united throughout so as to look like a 
single misshapen kidney with two or more pelves and irregular h\oo(\ 
vessels. The united kidneys may be both situated on one side of the 
vertebral column or in the pelvis. 

CHANGES IN POSITION. 

The kidlieys maybe pbiced in an abnormal siiuation, in which 
tliev are either fixed or movable. 



544 THE URINARY APPARATUS. 

The change in position is either lateral or downward. When 
displaced downward the kidney may be over the sacrum or below 
this in the cavity of the pehds. The vessels also have an irregular 
origin and distribution. The kidney is firmly attached in its abnor- 
mal position. 

Movable or wandering kidneys are found in adult life as a result 
of tight lacing, of pregnancy, of overexertion, and of unknown 
causes. They are more frequent in females than in males. The 
right kidney is the one more frequently affected. The blood vessels 
become lengthened and the attachments of the kidney longer and 
looser. 

bright's disease. 

This name is used as a convenient term to group together a cer- 
tain number of diseases of the kidney. This group may be subdi- 
vided as follows : 

I. Acute B right's Disease. 

1. Acute Congestion of the Kidney. 

2. Acute Degeneration of the Kidney. 

3. Acute Exudative Nephritis. 

4. Acute Diffuse Nephritis. 

II. Chronic Bright' s Disease. 

1. Chronic Congestion of the Kidney. 

2. Chronic Degeneration of the Kidney. 

3. Chronic Diffuse Nephritis ivith Exudation. 

4. Chronic Diffuse Nejjhritis tvithout Exudation. 

I. Acute Brighfs Disease. 

1. Acute Congestion of the Kidney. — This change in the kid= 
neys we know rather from clinical than from anatomical experi- 
ence. 

It is caused by the ingestion of some poisons, especially cau- 
tharides, by severe injuries, and by surgical operations. It also 
occurs as a temporary condition in the course of chronic Bright^s . 
disease. 

The characteristic symptom is diminution in the quantity, or sup- 
pression, of urine. ' 

2. Acute Degeneration of the Kidney. — This is an acute 
change in the kidneys, characterized by degeneration or death of the 
epithelium of the tubes and of the capsule cells of the glomeruli. It 
is also called ' ' parenchymatous degeneration. " 

It is caused by severe inflammations of other parts of the body; 
by the presence in the body of the poisons of the infectious diseases; 



THE URINARY APPARATUS. 



64:1 



and by the ingestion of poisons, especially of arsenic, mercury, and 
phosphorus. 

After death the gross appearance of the kidneys varies with the 
intensity of the morbid process and with the presence or absence of 
secondary changes on the part of the blood vessels. In the milder 
cases the kidney is a little swollen and the cortex is pale ; in the se- 
vere cases the kidney is much enlarged and the cortex is either white 
or congested. 

The changes in the renal epithelial cells are : a simple swelling of 
the cell body, especially of its network, causing it to look larger and 
more opaque and to take on irregular shapes ; an infiltration of the 

















Fig. 258.— Acute Degeneration of the Kidney (Acute Parenchymatous Degeneration'). 
From a case of yellow fever, a, the swollen and granular epithelium peeling otT and disinte- 
grating; b, hyalin material in the lumen of the tubule. 

cell bodies with granules of albuminoid matter and fat ; a deatli oL 
the cells, which may take the form of coagulation necrosis or of a 
disintegration and crumbling of the cell bodies ; a descpiamatiou of 
the dead cells ; a formation of hyalin masses in the cells ; a growtli 
of new cells to take the place of the dead epithelium. All these 
clianges are most marked in the convoluted tubes (Fig. ^loS"*. 

If the degeneration or death of the renal epithelium is extensive 
and produced (piickly, it is often accompanied by cc^ngestiou of t\w 
blood vessels and exudation of serum. The congestion will bt» finmd 
after death, and also casts in ihe straiu'ht tubules. 



64:6 



THE URIXAET APPARATUS. 



o 
O. 



Acute Exudative Xephritis. — This is fre<:iueiitly a prioiary 
nephritis, either occmriag after exposure to cold or without discov- 
erable cause. It coniphcates scarlatina, measles, diphtheria, typhoid 
fever, acute general tuberculosis, pneumonia, acute endocarditis. 
acute peritonitis, dysentery, erysipelas, diabetes, and many other of 
the infectious diseases and severe infla m mations. It is c^ne of the 
forms of nephritis which comphcate the puerperal condition. It has 
been observed in local epidemics, apparently due to the presence of 
pathogenic bacteria in the kidney. 





/i 



1.1 

iM 
H 



ll 



Ite. S9.— AC7TZ yEPHBTHS, X SO and rednccd. 
Paris zr^r- : ~e:irr hoars before death. 



';;■•! 



/ 



/■ 



The neohiitis has the ordinarv characters of an exudative indam- 
niarl'jn : cc-ngestion. an exudation of blood plasma, an emigration of 
white blood cells, and a diapedesis of red blood cells : to which may 
be added s^velling or necrosis of the renal epithehum and changes in 
the glomeruli. 

In the milder cases ^^e find the inflammatory products — serum, 
casts, Tvhite and red blood cells — in the urine. But in the kidneys 
after death we find no lesions, unless it may be a few casts in the 
straight tubes. The morbid process is confined to the blood vessels 



THE URINARY APPARATUS. 



547 



of the kidney, and its only result is the exudation into the renal 
tubules. 

In the more severe cases we find the kidneys large and smooth, 
the cortex thick and white, or white mottled with red, or the entire 
kidney intensely congested. If the stroma is infiltrated with serum 
the kidney is succulent and wet ; if the number of pus cells is very 
great there will be little, whitish foci in the cortex. 

There are, besides the exudation, changes in the tubes, the stroma, 
and the glomeruli. All the changes are most marked in the cortical 
portion of the kidney. 




P Q. 

Fig. 260.— Acute Nephritis occurring with Acute General Tuberculosis, X 850 and reduced. 



In the tubes the epithelium may be flattened, or swollen, opaque, 
and detached from the walls of the tubes. There may be a uniform, 
symmetrical dilatation of all the cortex tubes. The tubes may be 
empty or they may contain coagulated matters in the form of irregu- 
lar masses and of hyalin cylinders. The irregular masses are foimd 
principally in the convoluted tubes ; thoy seem to be formed by a 
coagulation of substances contained in the exuded blood plasma, ami 
are not to be confounded with the hyalin globules so often found in 
normal convoluted tubes. 



548 



THE URINARY APPARATUS. 



The hyalin cylinders are more numerous in the straight tubes, 
but are also found in the convoluted tubes. They are also formed 
of matter coagulated from the blood plasma, and are identical with 
the casts found in the urine. The tubes may also contain red and 
white blood cells. 

In some cases there is an excessive emigration of white blood 
cells. This excessive emigration is not necessarily attended with 
exudation of the blood serum, and so the urine of these patients may 
contain no albumin. 




<*■ 






)^'^ 



/ 



Fig. 261.— Acute Nephritis. 

Showing the swelling and growth of cells in and on the capillaries of a glomerulus in a case 
of scarlatina. 



The white blood cells are not found equally diffused throughout 
the kidney, but are collected in foci in the cortex. These foci 
may be very minute or attain a considerable size. They do not 
resemble the suppurating foci seen with embolism or with pyelo- 
nephritis. 

In the glomeruli we find considerable changes. The cavities of 
the capsules may contain coagulated matter and white and red 
blood cells, just as do the tubes. The capsular epithelium may be 
swollen, sometimes so much so as to resemble the tubular epithe- 



THE URINARY APPARATUS. o49 

lium, and this change is most marked in the capsular epithehum 
near the entrance of the tubes. 

The most noticeable change, however, is in the capillary tufts 
of the glomeruli. These capillaries are normally covered on their 
outer surfaces by flat, nucleated cells, so that the tuft is not made up 
of naked capillaries, but each separate capillary throughout its en- 
tire length is covered over' with these cells. There are also fiat cells 
which line the inner surfaces of the capillaries, but not continuously 
as is the case with capillaries in other parts of the body. 

In exudative nephritis the swelling and growth of cells on and in 
the capillaries change the appearance of the glomeruli. They are 
larger, more opaque ; the outlines of the main divisions of the tufts 
are visible, but those of the individual capillaries are lost. This 
change in the appearance of the glomeruli is due to the swelling and 
growth of the cells on and in the capillaries (Fig. 201). 

In very severe cases the growth of the cells on the tufts is so 
considerable that they form large masses of cells between the glo- 
merulus and its capsule. 

The walls of the arteries in the kidneys may be thickened by a 
swelling of their muscular coats. 

Acute exudative nephritis is regularly a transitory lesion. It 
may, indeed, be so severe as to destroy life in a short time. But, as 
a rule, if the patients do recover from it they recover completely 
and the kidneys return to their natural condition. 

4. Acute Diffuse Nephritis. — This is the most serious and im- 
portant of all the forms of acute nephritis, not only for the reason 
that it involves so much of the structure of the kidney, but because 
its lesions are from the first of a permanent character, and because 
disturbances of the general circulation are so frequently associated 
with it. 

It is one of the forms of scarlatinal nephritis ; it occurs early and 
late in the course of diphtheria ; it is the most important variety 
of the nephritis of pregnancy, and it is especially frequent as a pri- 
mary nephritis, with or without a history of exposure to cold. The 
course of the inflammation is acute or subacute. If it does not prove 
fatal as an acute inflammation it regularly continues as a chronic 
neplu'itis. 

The changes in the kidneys are extensive and well markod. 

The kidney's are large, at first smooth, later sometimes a little 
roughened ; the cortical portion is thick, white, or mottled with 
yellow or red, or congested ; the pyramids are red. 

In these kidneys wo find the same lesions as have been described 
as belonging to exudative nephritis, but with twt) additional clianges 
— changes which are found in the earliest stages of the intlanuna- 
49 



550 



THE URINARY APPARATUS. 



tion, and which give the characteristic stamp to the lesion : first, a 
group of connective tissue in the stroma ; second, a growth of the 
capsule cells of the glomeruli. 

These changes do not involve the whole of the kidney, but sym- 
metrical strips or wedges in the cortex, which follow the line of the 
arteries. These wedges are small or la-rge, few or numerous, regu- 
lar or irregular^ in the different kidneys. But in every wedge we 
find the same general characters : one or more arteries, of which 
the walls are thickened ; glomeruli belonging to these arteries, with 
a large growth of capsule cells compressing the tufts ; a growth of 
new connective tissue in the stroma around and parallel to the 




Fig. 262.— Acttte Diffuse Nephritis. 

From a case of scarlatina, a, swollen capsular epithelium; 6, proliferation of tuft cells; c, 
compressed tuft; d, swollen stroma infiltrated with cells; e, dilated convoluted tubules; g, swollen 
epithelium peeling off; 7i,hyalin casts. 

arteries. Between the wedges we find at first only the changes of 
exudative nephritis ; later, a diffuse growth of connective tissue 
(Fig. 262). ^ ^ ^ • 

If the nephritis is of acute type and recent the new tissue be- 
tween the tubes consists largely of cells ; if the nephritis is of sub- 
acute type and longer duration the tissue is denser and has more 
basement substance. Where the growth of new tissue is abundant 
the tubes become small and atrophied. 

The exudation from the blood vessels is ver}" considerable, so 
that the urine contains large quantities of albumin, many casts, and 
red and white blood cells. 



THE URINARY APPARATUS. 'J-jl 

TI. Chronic Brighfs Disease. 

1. Chronic Congestion of the Kidney. — This change in the kid- 
ney may be produced by any causes which interfere with the circu- 
lation of the blood and produce venous congestion. The most com- 
mon cause is valvular disease of the heart. 

The kidneys are of medium size or large. Their weight is in- 
creased ; they are hard and uniformly congested ; their surfaces are 
smooth. The epithelium of the cortex tubes is opaque, flattened, or 
swollen. The glomeruli show a dilatation of the capillaries, with 
more or less thickening of their walls, and swelling of the cells which 
cover their walls. In the stroma there is nothing but some exag- 
geration of the subcapsular areas of connective tissue which are 
found in normal kidneys. The arteries are normal, the pyramid 
veins are congested and sometimes dilated. 

The effect of this lesion of the kidney is simply to diminish the 
quantity of the urine, its quality remaining good. 

2. Chronic Degeneration of the Kidney. — This condition is 
produced by long-continued disturbances of the circulation due to 
heart disease, empyema, and similar conditions, and to causes which 
impair the general health, such as alcoholism. 

The kidneys are, as a rule, considerably increased in size, weigh- 
ing together f.rom sixteen to twenty ounces, but occasionally their 
size is much diminished. Their surfaces are smooth ; the cortical 
portion is thickened, of pink or white color ; the pyramids are red. 

The epithelium of the cortex tubes is swollen, coarsely granular, 
or infiltrated with fat. If the kidnej" lesion is due to disturbances of 
the circulation the capillaries of the glomeruli are dilated. There 
are no changes in the stroma or arteries. At times there is a small 
exudation from the blood vessels, and casts and albumin appear in 
the urine. 

These changes in the kidney do not, as we might expect, change 
materially the composition of the urine. This continues to contain 
its full relative quantity of solid matter. 

It is very difficult to find a satisfactory plan of classifying the 
remaining forms of chronic Bright's disease. The changes found in 
all the kidneys are of much the same Idnd, although differing in de- 
gree. The clinical symptoms also are of much the same character in 
all the patients. And yet it has alwa^'S been felt by clinical observ- 
ers that there are three main forms of chronic Bright's disease, and 
that there must be anatomical differences to correspond to these foi-nis. 

It has seemed to me that the simplest form of classifying these 
kidneys is according to the presence or absence of exudation from 



552 THE URIXARY APPARATUS. 

the blood vessels, and that, of the non-exudative cases, we may dis- 
tinguish the more active and the very slow cases. In this way we 
may speak of chronic diffuse nephritis with exudation ; chronic dif- 
fuse nephritis without exudation ; and chronic diffuse nephritis of 
very slow development. 

3. Chronic Diffuse Nephritis tvith Exudation. — This follows 
acute and subacute diffuse nephritis and chronic degeneration of the 
kidney, or it is from the first a chronic lesion. 

There is a certain activity about the morbid process, although 
the patients may not die until after a number of years. The dis- 
position to dropsy, to anaemia, to loss of flesh and strength, is very 
marked. 

The specific gravity of the urine is low, but yet often not below 
1020. The excretion of urea is diminished. The quantity of urine 
is increased, except at the times when the kidney is congested. 
Albumin in large quantities is present, except at the times when the 
inflammation seems nearly to have subsided. White and red blood 
cells are present from time to time when the nephritis becomes 
more intense. 

Most of the kidneys are increased in size. The surface is smooth 
or roughened, or nodular. The cortex is thick and white, or gray, 
or mottled with various combinations of v/hite, yellow, gray, and 
red. Less frequently the kidneys are small, the cortex is thick, 
white or gray. Occasionally the size and gross appearance are 
hardly to be distinguished from those of a normal kidney. 

The changes in the kidney are : a large exudation from the blood 
vessels, most of which is mixed with the urine, while a part is found 
in the kidney tubules in the form of coagulated matter and casts ; 
degeneration of the renal epithelium ; a growth of new connective 
tissue in the stroma between the tubes ; swelling and multiplication 
of the tuft cells of the glomeruli ; obliteration of the capillaries of 
the glomeruli, sometimes waxy degeneration of these capillaries. In 
a considerable number of these kidneys the walls of the arteries are 
thickened or the seat of waxy degeneration. 

As regards the exact detail of the development of these changes, 
the variety is almost without limit. The more ordinary types of the 
lesion are as follows : 

(a) The kidneys are changed as they are in acute diffuse nephri- 
tis. There are the same cortical wedges containing new connective 
tissue, atrophied tubes and glomeruli, arteries with thickened walls, 
and glomeruli with a new growth of capsule cells. Between the 
wedges the tubes are more or less dilated ; their epithelium is flat- 
tened ; there is a diffuse growth of connective tissue in the stroma ; 
the tuft cells of the glomeruli are increased in size and number. 



THE URINARY APPARATUS. 



553 



(h) There is a diffuse growth of connective tissue in the stroma 
of the cortex. The tubes are more or less dilated, their epithelium is 
flattened. The tuft cells of the glomeruli are increased in size and 
number. 

(c) There are irregular areas, just beneath the capsule, composed 
of connective tissue, atrophied tubes, and atrophied glomeruli. In 
the cortex between these areas there are more or less degeneration of 
the epithelium, irregula.r thickening of the stroma, deformities of the 
tubes, growth of tuft cells, and atrophy of the glomeruli. 

(d) There is waxy degeneration of the glomerular capillaries and 
arteries added to the other lesions. 




Fig. 2C3.— Chronic Diffuse Nephritis. 

Atrophied kidney, showing small patch of new connective tissue with atrophy of enclosed tubules, 
a, new connective tissue; 6, atrophied tubule containing hyalin cast; c, tubule with epithelium 
peelinjic off; (/, thickened capsule of glomerulus. 

(e) In addition to the other lesions there is extravasated blood in 
the tubes. 

4. Chronic Diffuse Nephritis icithout Exudation. — The ditVor- 
eiice between the more rapid and the very slow forms of chronic 
nephritis without exudation is a clinical one. The lesions ai-e the 
same in both sets of cases. 

In the more rapid cases the ordinary sjmiptoms are loss of llosh 
and strength, dj^spnoea, contraction of the arteries, hoadache, sleep- 
lessness, convulsions, and coma. The clinical history extends over a 



554 



THE URINARY APPARATUS. 



few months or over many years. The urine is generally abundant 
and of low specific gravity and without albumin. At the times when 
the patient is worse the urine is apt to be diminished and to contain 
a little albumin. 

In the slow cases there may be no symptoms, except a gradual 
fall in the specific gravity of the urine, up to the time of the patient^s 




Fia. 864.— Chronic Nephritis without Exudation. 
An atrophied glomerulus. 



death ; or from time to time some of the symptoms just mentioned 
are developed. 

After death many of these kidneys do not differ in their gross a]3_ 
pearance from normal kidneys. If the disease is far advanced, how_ 
ever, most of them are atrophied, with adherent capsules and nodu- 
lar surfaces. Less frequently these kidneys are very large. 

The most prominent feature of the lesion is the growth of new 
connective tissue in the stroma (Fig. 263). This is confined to areas 



THE URINARY APPARATUS. 



000 



of irregular shape "in the cortex, or there is also a diffuse growth of 
connective tissue in the cortex and in the pyramids. 

The epithelium of the tubes is degenerated. Where there is 
much new connective tissue the tubes are atrophied and compressed. 
In other places the tubes are irregularly dilated, sometimes so much 
so as to form cysts. 

Of the glomeruli, some have their capsules thickened, some show 
a swelling and growth of the tuft cells, some are atrophied (Fig. 
264) ; in some the capillaries undergo waxy degeneration (Fig. 265). 

There are very often changes in the arteries. There may be only 




Fig. 265.— Waxy Degeneration of Tuft Capillaries. 
a, the tuft is completely transformed into a waxy mass; 6, portions of tuft waxy; c, tuft ca- 
pillaries normal ; d , convoluted tubule with disintegrating epithelium. 

thickening of the muscular coat, with no change in the size of the lu- 
men of the artery. There may be a diffuse connective-tissue thick- 
ening of the entire wall of the arter}-, with moderate diminution of 
its lumen. There may be thickening of the inner coat, so great as 
partly or completely to close the artery. 



SUPPURATIVE NEPHRITIS AND PYELO-NEPHRITIS. 

Suppurative inflammation of the kidney may bo produced by in- 
juries, by infectious emboli, by cystitis, and may occur Avithout dis- 
coverable cause. 



556 THE URIXARY APPARATUS. 

1. Suppurative Nephritis from Injury. — Gunshot wounds, in- 
cised or punctured wounds, falls, blows, and kicks are the ordinary 
traumatic causes. If the injury is a very severe one it usually 
causes the death of the patient in a short time ; if it is less severe, 
suppurative inflammation is developed. The inflammatory process 
may be diffuse, so that nearly the whole of one or of both kidneys 
is converted into a soft mass composed of pus, blood, and broken- 
dc^m tissue ; or it is circumscribed and one or more abscesses are 
formed in the kidney. 

2. Embolic Abscesses. — In pysemia and in malignant endocardi- 
tis small infectious emboli find their way into the arteries of the 
kidneys and produce necrosis of small areas of tissue, with surround- 
ing zones of suppurative inflammation. The entire kidney is en- 
larged and congested, and is dotted with little white foci surrounded 
by red zones. The foci are formed by an infiltration of pus cells be- 
tween the tubes, with more or less degeneration of kidney tissue. 
Colonies of micrococci are sometimes, but not always, found in the 
Malpighian tufts and in the abscesses (see Figs. 48 and 49). 

3. IdiojDathic Abscesses. — Sometimes abscesses of one or both 
kidneys are met with which have existed for a long time and for 
which no cause can be discovered. After death the kidney is found 
changed into a sac full of pus and surrounded by fibrous tissue. 
The pelvis and calyces are dilated and their walls are thickened. 
The connective tissue around the kidney, and its capsule, are also 
thickened. Suppurating sinuses ma}' extend from the kidney into 
the surrounding soft parts. 

4. Suppurative Pyelo-Xephritis with Cystitis. — Both kidneys 
are usually affected. The mucous membrane of the peh4s is con- 
gested, thickened, and coated with pus or T^-ith patches of fibrin. 
Scattered through the kidneys are abscesses and foci of pus of dif- 
ferent sizes. The smallest are hardly visible to the naked eye, but 
with the microscope we find small collections of pus cells between 
the tubes, mth swelling and degeneration of the renal epithelium. 
The larger purulent foci look like white streaks or wedges parallel 
to the tubes and surrounded by zones of congestion. The larger 
abscesses replace considerable portions of the kidney tissue. 

The ureters are sometimes inflamed, their walls are thickened, 
their inner surfaces are coated with pus or fibrin. 

The bladder is always inflamed, and this is the primary lesion, to 
which the kidney lesion is secondary. It may present any of the 
lesions of acute or chronic cystitis. 

CHRONIC PYELO-XEPHRITIS. 

Chronic cystitis or calculi in the pelvis of the kidney may set up 



THE URINARY APPARATUS. 5o7 

a chronic inflammation which involves both the pelvis and calyces 
and the kidney tissue. The mucous membrane of the pelvis and 
calyces is thickened, the epithelial layer is changed, there is a growth 
of granulation tissue beneath the epithelium, and there may be little 
polypoid outgrowths. The surface of the mucous membrane is 
coated with pus or fibrin, or the cavity of the pelvis is dilated and 
distended with purulent serum. 

The kidney itself is the seat of a chronic interstitial inflammation 
with the production of new connective tissue, and sometimes of pus, 
with obliteration of the renal tubules. 

TUBERCULAR NEPHRITIS. 

This lesion is usually, though not always, associated with tuber- 
cular inflammation in other parts of the genito-urinary tract. 

It is usually unilateral, occurring most frequently on the left side. 
The process may commence in the kidney or in some other part of 
the genito-urinary tract. If only one kidney is involved the other is 
apt to become the seat of chronic diffuse nephritis with waxy de- 
generation of the walls of the arteries. The tubercular inflamma- 
tion may occur in a kidney already the seat of chronic inflammatory 
changes. 

The lesion seems to begin in the mucous membrane of the peh^s 
and calyces, and extends from thence first to the pyramidal and after- 
ward to the cortical portion of the kidneys. In the mucous mem- 
brane of the pelvis and calyces there is a growth of granulation 
tissue studded with tubercle granula in the stroma, while the epithe- 
lial cells proliferate, become deformed, and desquamate. This pro- 
cess is often rapidly succeeded by cheesy degeneration of all the in- 
flammatory products. 

In the kidney there is the same production of granulation tissue 
and tubercle granula, which soon undergo cheesy degeneration, the 
degeneration involving the adjacent kidney tissue. In addition to 
this there is in the rest of the kidney chronic interstitial or suppura- 
tive inflammation. So the entire kidney is enlarged, portions are in 
the condition of cheesy degeneration or have sloughed away, while 
the rest of the kidney is dense and hard. Or, if suppuration takes 
place, the kidney is hollowed out into cavities filled with cheesy mat- 
ter and pus. 

Sometimes the process comes to a standstill, and then the choesy 
portions are infiltrated with salts of lime. 

EMBOLISM AND THROMBOSIS. 

Acute and chronic endocarditis affecting- the left side of the heart, 
and chronic endarteritis of the aorta, frequently rosuh in the forma- 



558 THE URINARY APPARATUS. 

tion of vegetations, portions of which become detached and lodged as 
emboH in the branches of the renal artery. 

The occlusion of an artery in this way produces in the kidneys 
wedge-shaped infarctions, varying in their size with the size of the 
obstructed artery. The infarction loses the natural red color of the 
kidney and becomes first yellow and then white. The renal epithe- 
lium degenerates and disappears, the tubes become collapsed and 
shrunken ; around the infarction is a zone of congestion and of infil- 
tration with pus cells. After this the infarction becomes shrunken, 
dense, and changed into connective tissue. The kidney is then left 
deformed by the cicatricial depressions and contractions. It is pos- 
sible, however, for the infarction to become gangrenous, or to be 
surrounded by a zone of purulent infiltration, and break down so as 
to form an abscess. Rarely the infarctions are of the hsemorrhagic 
variety. 

Embolism of the trunk of the renal artery produces complete ne- 
crosis of the kidney. 

Infectious emboli are small and produce little purulent foci (see 
above). 

Thrombosis of the renal vein and its branches may occur in pa- 
tients suffering from chronic Bright^s disease.' It can also be pro- 
duced by tumors pressing on the veins, by thrombi of the vena 
cava, and occurs as a primary lesion dependent on the general con- 
dition of the patient. 

HYDRONEPHROSIS. 

Dilatation of the pelvis and calyces of the kidneys is found as a 
congenital condition. In some cases other malformations, such as 
club-foot, hare-lip, and imperforate anus, are also present. The pel- 
ves and calyces of both kidneys, and the ureters, are distended with 
urine ; the bladder is also distended and its wall may be hypertro- 
phied. The urethra may be closed, or no obstruction can be demon- 
strated. In these latter cases it is supposed that there does exist 
some membranous obstruction, which is broken by the probe or 
catheter used to explore the urethra. 

In adult fife hydronephrosis is produced by mechanical obstruc- 
tion of the urethra or ureters, due to inflammation, tumors, or 
calcuh. According to the position of the obstruction, either one or 
both kidneys are involved. 

The pelvis and calyces are dilated, sometimes enormously, and 
filled with urine alone or urine mixed with pus. The kidney tissue 
is flattened and thinned over the distended cavities. Its texture may 



Moxon, Trans. Lond. Path. Society, 1870, p. 248. 



THE URINARY APPARATUS. 



650 



remain unchanged, or there may be developed suppurative pyelo- 
nephritis or chronic diffuse nephritis. 

THE CYSTIC KIDNEY. 

Cysts are formed in the kidneys, both during intra-uterine and 
extra-uterine life. 

The congenital cystic kidney is a very remarkable pathological 
condition. Either one or both kidneys are enormously enlarged and 
converted into a mass of cysts. The cysts are of all sizes and are 
separated from each other by fibrous septa or compressed kidney tis- 




FiG. '-266.— Cysts op Kidney. 

sue. They contain a clear yellow, acid fluid holding in solution 
the urinary salts. Or the fluid is turbid and brown, and contains 
blood, uric acid crystals, and cholesterin. The cysts are lined with 
a single layer of flat, polygonal cells. They seem to be formed by a 
dilatation of the tubules and of the capsules of the ]\Ialpighian bodies. 
As causes for such dilatations are found obliteration of the tubes in 
the papilbB, and stenosis of the pelvis, ureters, bladder, or urethi-a. 
Other congenital malformations are of ten associated with this one.' 
In adult life we find three varieties of cystic kidney : 
1. In kidneys which are otherwise normal there are one or more 

' Vircb., Ges. Abhaudl. 



560 THE URINARY APPARATUS. 

cysts filled with clear or orown serum or colloid matter. These ^ 
cysts do not appear to interfere at all with the function of the kid- 
neys. 

2. In chronic diffuse nephritis, especially in the atrophic form, 
groups of tubes are dilated. Apparently one or more of the larger 
tubes in the pyramids is obstructed, and this causes dilatation of a 
corresponding group of tubes. Such a dilatation may be moderate 
in size, or it may form cysts visible to the naked eye. 

3. Both kidneys are very much enlarged and converted into a 
mass of cysts containing clear or colored serum or colloid matter. 
The nature of these cysts is uncertain. It is possible that they are 
congenital. They are sometimes associated with similar cysts in the 
liver. They seem to produce no renal symptoms until shortly before 
the patient's deaths unless chronic nephritis also exists, and then 
there are the ordinary symptoms of chronic Bright's disease. 

PERINEPHRITIS. 

The loose connective tissue which is situated around and beneath 
the kidney may become the seat of suppurative inflammation, and in 
this way abscesses of considerable size are formed. 

Such a perinephritis may be either secondary or primary. The 
secondary cases are due to extension of the inflammation from ab ■ 
scesses in the vicinity, such as are formed with caries of the spine, 
pelvic cellulitis, puerperal parametritis, perityphlitis, and suppura- 
tive nephritis. 

The primary cases occur after exposure to cold, after contusions 
over the lumbar region, and after great muscular exertion ; or no 
cause can be discovered. 

Complicating cases occur in the course of typjius and typhoid 
fevers and of small-pox. 

Most of the reported cases have been in persons between the ages 
of twenty and forty years. Less frequently children and older per- 
sons are affected. 

In the idiopathic cases the connective tissue behind the kidney 
seems to be the point of origin of the inflammatory process, and it is 
here that the pus first collects. After the abscess has formed the 
suppuration extends and the pus burrows in different directions : 
backward through the muscles ; downward into the iliac fossa, the 
perineum, the bladder, the scrotum, or the vagina ; forward into 
the peritoneal cavity or the colon ; upward through the diaphragm. 

The kidney itself is simply compressed by the abscess, or its tis- 
sue becomes involved in the suppurative inflammation. 



THE URINARY APPARATUS. O^il 



RENAL CALCULI. 



In the kidneys of new-born children, from the first to the four- 
teenth day after birth, the large tubes of the pyramids often con- 
tain small, brownish, rounded bodies composed of the urates of am- 
monium and sodium. Similar masses may also be present in the 
calyces and pelves. In still-born children these masses are usually 
absent. The carbonate and phosphate of lime may be deposited in 
the tubes of the pyramids, in the form of white linear masses, in the 
kidneys of old persons and of those who have suffered from destruc- 
tive diseases of the bones. 

Urate of soda in the form of acicular crystals is deposited both in 
the tubes and stroma of the kidneys of gouty persons. 

Concretions of the urinary salts are often formed in the pelves of 
the kidneys. They may remain there as rounded masses, or they 
may attain a large size and be moulded into the shape of the pelvis 
and calyces. Smaller calculi may pass into the ureter and either 
become impacted there or pass through it into the bladder. The 
most common form of calculus is that composed of uric acid. But 
they may also be formed of uric acid with a shell of oxalate of lime, 
or of oxalate of lime alone, or of the phosphates, or of cystin. 

The most serious result of the presence of these calculi is the oc- 
clusion of the ureters or the production of pyelo-nephritis. 

TUMORS. 

Fibroma. — Small, hard, white fibrous nodules are frequently 
found in the pyramids. They are of no special importance. Tliey 
may be mistaken for miliary tubercles. Large fibromata are very 
rare. ^ 

Lipoma. — Small fatty tumors are found in the cortex of the kid- 
ney just beneath the capsule. They are composed of fully devel- 
oped fat tissue. The fat is developed in the stroma so as to replace 
the kidney tissue.'^ 

Papilloma. — Villous tumors, formed of tufts of connective tissue 
covered with epithelium, may grow from the mu(X)us membrane of 
the pelvis.^ A peculiar form of papillary and cystic growth of the 
ureter is described.'' 

Myxo-Sarcoma. — Large tumors may grow from the pelvis of tlie 
kidney. They are not simple myxoniata., but are composed of mu- 
cous tissue, fat, and sarcomatous tissue. 



> Wilts, Trans. Lond. Path. Soc, xx. 
- Virckoic, " Krank. Geschwiilste." Bd. i., p. ;}85. 
'Trans. Lond. Path. Soc, 1870. p. '2'Sd. 
^Vn-ch. Arch., Bd. Ixvi., p. 139. 



562 THE URINARY APPARATUS. 

Myoma. — Small tumors comiposed of smooth muse alar fibres and 
of round cells are found in the cortex close to the capsule. 

A tumor composed of striated muscle and round cells is described 
by Cohnheim/ 

A tumor composed partly of smooth muscle, partly of striped 
muscle, and partly of sarcomatous tissue is described by Eberth/ 

Angioma cavernosum occurs in the form of small nodules situ- 
ated in the cortex. 

Lymphoma. — Small white tumors composed of tissue like that of 
the lymphatic glands are found in cases of leukaemia and pseudo- 
leuksemia. Less frequently they are found with typhoid fever, scar- 
let fever, and diphtheria. 

Adenoma. — This form of tumor is situated in the cortex of the 
kidney and may invade the pyramidal portion also. Usually there is 
only a single tumor, but sometimes two or more, or they may even 
occur in both kidneys. They vary in size ; some are not larger than 
a pea, others are as large as a hen's egg. They are of rounded form, 
of whitish color, and separated by a capsule from the kidney tissue. 
The tumors are most frequent in persons over forty years of age. 

There are two principal varieties of these tumors, the papillary 
and the alveolar. 

1. The Papillary Adenoma. — There are cavities of different 
sizes, from the walls of which spring branching tufts covered with 
cylindrical or cuboidal epithelium. These tufts nearly fill the cavi- 
ties. 

2. The Alveolar Adenoma. — There is a connective-tissue frame- 
work enclosing small round, oval, or tubular alveoli, lined or filled 
with cells. The cells are large, polygonal, nucleated bodies. 

The adenomata frequently undergo fatty degeneration, which 
may be so complete that they look like fatty tumors. 

Or there may be an excessive development of the stroma, with 
atrophy of the epithelial cells. 

There may be an excessive development and dilatation of the ca- 
pillaries and veins in the stroma. 

Cysts of considerable size may be formed by dilatation of the cavi- 
ties or alveoli.^ 

There are larger tumors, involving the whole of the kidney and 
accompanied with metastatic growths in other parts of the body, 
which have the same structure as the papillary adenomata. 

A congenital adenoma is described by Weigert.^ 



1 Virch. Arch., Bd. Ixv., p. 64. 

2 Ibid., Bd. Iv., p. 518. 

2 Medizinisch. Jahrb., 1883, p. 213, Virch. Arch., Bd. xciii., p. 89. 

4 Virch. Arch., Bd. Ixvii., p. 492. 



THE URINARY APPARATUS. oO'i 

Carcinoma. — Besides secondary carcinoma of the kidney there is 
also a primary form. Our knowledge of this has been much ob- 
scured by confounding with it adenomata and sarcomata. 

There seems to be, however, a real epithelial growth, originating 
in the kidney tubules, which forms tumors of large size and malig- 
nant character. 

Sarcoma. — Tumors formed of connective-tissue cells may origi- 
nate either in the pelvis of the kidney or in the kidney itself. They 
form tumors of large size and malignant character. Those which 
grow from the pelvis are usually myxo-sarcomata. Those which 
originate in the kidney tissue reach a large size and are soft and 
hsemorrhagic. Their stroma forms irregular alveoli filled with small 
round cells. 

PARASITES. 

Echinococcus, in its ordinary form of ixiother and daughter cysts, 
is sometimes found in the kidney. The cysts may open into the pel- 
vis of the kidney, into the pleura, or through the wall of the abdomen. 

Cysticercus cellulosce is of very rare occurrence. 

Pentastomum denticulatum has been seen once by E. Wagner. 

Filaria sanguinis hominis is found in the arteries, veins, lym- 
phatics, and stroma. 

Strongylus gigas has been found several times in the pelvis of 
the kidney. 

THE URINARY BLADDER. 

MALFORMATIONS. 

Exstroversion of the bladder is one of the most frequent mal- 
formations, and may occur in either sex. It presents several varie- 
ties : 

1. The umbilicus is lower down than usual, the pubic bones are 
not united at the symphysis, the pelvis is wider and shallower than 
it should be. Between the umbilicus and pubes the abdominal wall 
is wanting. In its place is a projecting, ovoid mass of mucous mem- 
brane, in which may be seen the openings of the ureters. The penis 
is usually rudimentary ; the urethra is an open fissure (epispadias) ; 
the clitoris may be separated into two halves. The ureters usually 
open normally ; sometimes their openings are displaced or are multi- 
ple. They may be dilateel. 

2. There may be a fissure in the abdominal wall. lilloJ up bv 
the perfectly formed bladder. 

3. The umbihcus may be well formed, and there is a })ortiou of 
abdominal wall between it and the exstrophieil bladder. 

4. The external genitals and urethra may be well fornunl. aiul the 
symphj^sis pubis united, while onlv the bladder is tissured. 



564 THE URINARY APPARATUS. ^ 

5. The genitals, urethra, and symphysis may be well formed, the 
bladder closed except at the upper part of its anterior wall. The 
bladder is entirely or in part inverted and pushed through the open- 
ing in the abdominal wall. 

The Urachus normally remains as a very small canal, five to 
seven cm. long, with a small opening into the bladder, or entirely 
closed at that point. If there is a congenital obstruction to the flo^v 
of urine through the urethra, the urachus may remain open and the 
urine pass through it. 

Absence of the Bladder is of rare occurrence. The bladder may 
be very small, the urine passing almost directly into the urethra. 
The bladder may be separated into an upper and a lower portion by 
a circular constriction. It may be completely divided by a vertical 
septum into two lateral portions. Diverticula of the wall of the 
bladder are sometimes found in new-born children. Partial or com- 
plete closure of the neck of the bladder may occur. This may lead 
to hydronephrosis, or the urine may be discharged through the open 
urachus. 

CHANGES IN SIZE AND POSITION. 

Dilatation. — This may be general or partial, leading to the 
formation of diverticula. 

General dilatation of the bladder is produced by the accumulation 
of urine in consequence of some mechanical obstacle to its escape, or 
of paralysis of the muscular walls of the organ. The dilatation is 
usually uniform and may be very great, so that the bladder may 
reach to the umbilicus. If the walls of the bladder are paralyzed, or 
the obstruction occurs suddenly or is complete, the wall of the blad- 
der is thinned. When an incomplete obstruction exists for some 
time the walls of the bladder are apt to hypertrophy, so that, al- 
though the bladder is larger than normal, the walls may not only be 
of the usual thickness, but even very much thicker. In the foetus 
dilatation of the bladder may reach such a size as to interfere with 
delivery. 

The retained urine in dilated bladders is liable to decomposition, 
leading to inflammation or gangrene of the mucous membrane. 

Diverticula of the bladder may be produced by the pouching-out 
of circumscribed portions of the wall of the bladder, the wall of the 
pouch containing all the layers of the bladder wall. More frequently, 
however, they are produced by a protrusion of the mucous membrane 
between hypertrophied bundles of rauscle fibre. They may be very 
small, or they may be as large as a child's head. They may com- 
municate "vvith the bladder by a large or a small opening. The de- 
composition of stagnant urine in diverticula is apt to induce inflam- 



THE URINARY APPARATUS. o05 

mation. Calculi may be formed in them or may slip into them from 
the bladder. 

Hypertrophy of the muscular coat of the bladder is usually pro- 
duced by mechanical obstructions to the outflow (jf urine, such as 
stricture of the urethra, enlarged prostate, calculi, new growths, etc. 
The muscular coat is thickened uniformly or assumes a trabeculated 
appearance. The organ retains its normal capacity, or is dilated, or 
becomes smaller. The mucous membrane is frequently the seat of 
chronic or acute inflammation. Dilatation of the ureters and hydro- 
nephrosis frequently accompany this condition. 

Her nice of the bladder sometimes accompany intestinal hernite 
through the inguinal and crural canals and the foramen ovale. The 
changes in position of the bladder, produced by displacements of 
the vagina and uterus, will be mentioned with the lesions of th(jse 
organs. 

In the female the base of the bladder may press downward, caus- 
ing protrusion of the vaginal wall {vaginal cystocele) ; or there 
may be inversion and prolapse of bladder through the dilated 
urethra. 

RUPTURE — PERFORATION. 

Penetrating wounds of the bladder may permit escape of urine 
into the abdominal cavity, or infiltration into the surrounding con- 
nective tissue, or permanent fistulse. Such wounds are always seri- 
ous and frequently fatal, owing chiefly to the severe and often 
gangrenous inflammation which decomposing urine sets up in the 
connective tissue, or to the peritonitis induced by the same cause. 

Rupture of the bladder may be produced by severe blows and 
falls when the bladder contains urine. More rarely rupture takes 
})lace from overdistention. Death may occur from rupture of the 
bladder with escape of urine into the peritoneal cavit}-, without evi- 
dences of peritonitis. 

Perforations of the bladder are produced by ulceration and 
gangrene, by abscesses from without, and by cancerous ulceration 
from the adjoining organs. Fractures of the pelvic bones may pro- 
duce laceration of the bladder. Perforations of the bladder may 
lead to the establishment of fistuliB. communicating with the rectum, 
vagina, uterus, ov opening externally. 

DISTURBANCES OF TIROULATION. 

Hypenemia. — Aside from active hyperavniia of the mucous mem- 
brane in acute inflammation, the bladder is not infrequently the seat 
of chronic congestion from obstruction to the venous circulativ^u. 
Under these conditions there mav be chronic catarrhal intlamma- 
50 



566 THE URINARY APPARATUS. 

tion, or a marked dilatation of the veins (vesical hseniorrhoids), 
which may give rise to haemorrhage or to obstruction of the opening 
of the ureters. 

Hemorrhage. — Extensive hsemorrhages into the bladder are 
commonly due to injury or to the presence of calculi or tumors. 
Small haemorrhages into the substance of the mucous membrane may 
accompany inflammation, the hsemorrhagic diathesis, scurvy, pur- 
pura, small-pox, etc. If the haemorrhage is considerable and occurs 
rapidly in an empty bladder, a clot is apt to form ; but when the 
blood mixes with urine as it is extravasated it more commonly re- 
mains liquid and is discharged as a reddish-brown fluid. 

INFLAMMATION. 

Acute Catarrhal Cystitis. — This may be incited by the pre- 
sence of urine which has decomposed under the influence of bacteria ; 
by cantharides or other drugs ; by the presence of foreign bodies 
and calculi ; or it may be due to an extension of gonorrhoeal urethri- 
tis or vaginitis ; or it may occur without assignable cause. The 
mucous membrane is swollen and congested, although these altera- 
tions may not be very evident after death. The surfaces may be 
coated with mucus containing red blood cells and pus. The epithe- 
lium is apt to be loosened and in some places peeled off, so that 
superficial or deep ulceration may occur. We may find mixed with 
the urine in the organ shreds of mucus, pus cells, epithelial cells of 
various shapes, usually more or less swollen and granular, or frag- 
ments of such cells ; red blood cells and bacteria. Resolution may 
occur from acute catarrhal cystitis, but it very frequently assumes a 
chronic character. 

The small nodules of lymphoid tissue in the mucous membrane 
of the bladder, especially near the neck, may become enlarged and 
prominent in cystitis, and may then considerably resemble miliary 
tubercles. 

Chronic Cystitis. — In this form the mucous membrane may be 
swollen, succulent, grayish, or mottled with spots of congestion or 
extravasation, and covered with a layer of mucus and pus. Micro- 
scopically the membrane may be more or less infiltrated with pus 
cells, and pus may be constantly produced and thrown off into the 
urine. Later the mucous membrane may become thickened either 
diffusely or in the form of tufts or polypi. In some cases it becomes 
atrophied. Owing to decomposition of the haemoglobin in the extra- 
vasated blood the mucosa may become pigmented, brown, or slate- 
colored. The mucous membrane frequently becomes eroded, espe- 
cially on the most elevated portions, or deep ulcerations may occur. 
The muscular coats may become paralyzed and the bladder dilated ; 



THE URINARY APPARATUS. 56? 

or the submucosa or the muscularis, or both, may become hypertro- 
phiecl. The mucous membrane may become encrusted with urinary 
salts. 

In another class of cases the inflammation assumes a more in- 
tense and necrotic character. Larger and smaller shreds and patches 
of the mucosa die, become brown or gray in color, loosen or peel off, 
and become mixed with the urine and exudations. The gangrenous 
process may extend to all the coats of the bladder, so that perfora- 
tion and fatal 23eritonitis may occur. The gangrenous form of cys- 
titis is most apt to occur in paralytics. In still another class of cases 
the inflammation assumes a suppurative character. The submu- 
cosa, the intermuscular connective tissue, and the adjacent parts be- 
come infiltrated with pus, either diffusely or in the form of larger 
and smaller abscesses, which may open externally or internally, 
forming deep ulcers. In all these cases the inflammation may ex- 
tend to the ureters and kidneys ; it may skip the ureters and in- 
volve the kidneys. 

Croujpous Inflammation, — In connection Avith any of the above 
lesions the mucous membrane of the bladder may be covered, in 
patches or sometimes over a considerable portion of its surface, ^A^th 
a layer of fibrin, either granular or fibrillar, enclosing pus and epithe- 
lial cells and bacteria. The mucosa may be infiltrated with fibrin. 

This form of inflammation may occur in connection with severe 
infectious diseases — measles, diphtheria, scarlatina, typhoid fever : 
in connection with similar inflammation of the external genitals, in 
puerperal fever, noma, and sometimes in the presence of foreign 
bodies. It is rarel}^ an idiopathic disease. 

Tubercular Inflammation. — This disease commences by the for- 
mation of miliary tubercles in the mucous membrane of the bladder. 
By the coalescence of the tubercles and the degeneration of tissue 
about them, ulcers are formed, and it is most frequently in the ul- 
cerative stage that the lesion is seen. The ulcers, which may be 
large or small, are usually most abundant at the base of the organ. 
Their edges may be cheesy, and miliary tubercles in greater or 
smaller numbers are usually found in the mucosa about them. Xot 
infrequently large shreds of tissue are loosened and cast oft'. The 
mucosa about the ulcers is apt to be infiltrated with small spheroi- 
dal cells. Tubercle bacilli are present in many of the tubercles and 
in the edj2fes and base of the ulcers, Tliev mav also be found in the 
urine, and are then of diagnostic significance. Catarrhal inflannna- 
tion is a very constant accompaniment of this lesion. Tubercular 
cvstitis may occur in connection with tubercular infianunation of 
the lungs, intestines, or of the kidney, uterus. ])rostate. etc. 



568 THE URINARY APPARATUS. 

TUMORS. 

Fihromata have been described, occurring as small nodular tu- 
mors in the submucosa, but they are rare. 

Aside from the polypoid thickenings of the mucosa occurring in 
chronic cystitis, soft vascular papillomata are of frequent occur- 
rence. These tumors vary in size from that of a pea to that of a 
pigeon's egg or larger. They consist of a fibrous, often very vascu- 
lar stroma, and are covered on the surface with numerous small, 
closely set, villous projections, over which are irregular layers of 
elongated or cylindrical cells. These tumors are very liable to bleed, 
are often accompanied by vesical catarrh, and may be covered by a 
precipitate of urinary salts. The epithelium is liable to peel off from 
the surface of the villi and appear in the urine. Sarcoma of the 
bladder has been described. 

Carcino7na. — Carcinoma of the bladder is most frequently sec- 
ondary, and is then ra,rely due to metastasis, but usually to an ex- 
tension of the growth from neighboring parts, as the uterus^ vagina, 
or rectum. 

Primary carcinoma of the bladder may occur : 

1. As a diffuse scirrhous infiltration of the entire wall of the 
bladder, usually with ulcerations of its inner surface. 

2. As a circumscribed nodule which grows inward and out- 
ward, ulcerating on its inner surface, and sometimes producing per- 
forations. 

3. As villous or papillomatous groivth. The tumor grows 
from one or more points of the inner surface of the bladder. It is 
formed of tubular follicles lined with cjdindrical epithelium, and, 
on its inner free surface, of tufts covered with cylindrical epithe- 
lium. The new growth may involve the entire thickness of the wall 
of the bladder. 

4. A few cases of carcinoma have been described in which the 
stroma contained a varying quantity of smooth muscle tissue. ^ 

Cysts. — Dermoid cysts of the wall of the bladder have been de- 
scribed, but are rare. Small cysts with serous contents sometimes 
occur in the mucous membrane ; a part of them, at least, are be- 
lieved to be due to faulty embryonal development. 

PARASITES, ETC. 

Among the animal parasites occasionally found in the bladder 
may be mentioned JEchinococcus, Distoma hcematobium, Filaria 
sanguinis, Ascarides, and Oxyurides. 

^ The literature of tumors of the bladder may be found in Stein's ' ' Study of the 
Tumors of the Bladder," 1881. 



THE URINARY APPARATUS. 500 

Bacteria of various forms not infrequently occur in the Vjladder, 
particularly in connection with chronic cystitis. B. termo, Micro- 
coccus urece, and Sarcina may be mentioned as of most frequent 
occurrence. 

A great variety of foreign bodies may be found in the bladder, 
particularly in the female. If their stay is long they are apt to be- 
come encrusted with urinary salts. 

CALCULI. 

Vesical calculi may occur singly or in great numbers, and vary 
greatly in size, ranging from small, sand-like particles up to masses 
four or five inches in diameter, but the usual range is from the size 
of a pea to that of a hen's q^^. They are usually oval, spheroidal, 
or elongated ; or, when several are present, they are apt to be 
faceted. The surface may be smooth or rough. They are usually 
more or less distinctly lamellated, and are frequently formed around 
a central body called a nucleus, which may either be formed of 
urinary salts or some foreign body. Their most common constitu- 
ents are phosphates, uric acid and urates, and calcium oxalate ^ 
or various combinations of these. 

Uric Acid Calculi. — These are the most common of vesical cal- 
culi. In the form of small brownish-red, crystalline aggregations 
they may be passed as'' gravel." The larger uric acid calculi are 
not commonly of very great size, are frequently finely nodulated on 
the surface, but may be smooth. The color varies from light yellow 
to dark reddish-brown ; they are usually dense and lamellated. 

Calculi formed of Urates. — Calculi composed of pure urates 
are rare, these salts being more commonly combined Avith uric acid 
and the phosphates to form the complex calculi. Sodium urate, in 
the form of small spined, more or less globular crystalline masses, 
forms one of the varieties of '' gravel." 

Phosphatic Calculi. — Vnve calcium phosphate calculi are, rarely, 
found as whitish, usually smooth, and small lamellated concretions. 

Mixed or Triple Phosphate calculi are common, and frequently 
attain large size. These calculi are sometimes pure, but the deposit 
is more frequently associated with other salts, either as encrusting or 
intercalated lamelljTe. Triple phosphate calculi are usually rough on 
the surface, of grayish-white color, lamellated, and frequently very 
friable. 

Small gray or white, hard, and usually smooth calculi of pure 
calcium carlyouate occur rarely. Calcium carbonate is sometimes 
passed as gravel in the form of minute spheroidal bodies, either 
singly or in clusters. 

Calcium Oxalate c>alculi (nuilberry calculi) are comparatively 



570 THE URINARY APPARATUS. 

common, either pure or in combination with uric acid or the phos- 
phates. Calcium oxalate may occur in the form of very small, hard, 
smooth concretions, or as larger, heavy, hard, finely or coarsely 
nodulated brown or blackish lamellated masses. The nucleus or 
some of the lamellae, or both, are often composed of uric acid. 

Cystin Calculi are usually ovoidal in shape, of waxy consistence, 
of clear or brownish or greenish-yellow color, with mammillated 
surface and crystalline fracture. Cystin may be associated in a 
variety of ways with other calculi. 

Xanthin Calculi, which are very rare, are usually of moderate 
size, smooth, of a cinnamon or cinnabar-red color, lamellated, and 
oval or flattened in shape. 

Solid masses of fibrin and blood sometimes occur in the bladder, 
and may exist as independent structures, or form nuclei for the de- 
posit of urinary salts. 

For a detailed account of calculi, the conditions under which 
they form, modes of analysis, etc., we refer to special works on this 
subject. 

THE URETHRA. 
CONGENITAL MALFORMATIONS. 

Some of the malformations of the urethra are described with 
those of the penis. 

The urethra may be impervious or may open at the root of the 
penis. More commonly there is partial obliteration or stricture of 
some part of the canal. 

The entire urethra may be dilated into a sac full of urine. 

There may be a canal on the dorsum of the penis, formed by the 
fusion of the spermatic cords, and opening in the glans above the 
urethra. 

There may be two or more openings of the urethra. 

The canal may be dislocated so as to open in the inguinal re- 
gion. 

A number of cases have been reported in which a valve in the 
urethra has produced hypertrophy of the bladder, dilatation of the 
ureters, and hydronephrosis.^ 

Owing to its narrowness, greater length, and peculiar connec- 
tions with the internal generative organs, the male urethra is much 
more liable to disease than the female. 

CHANGES IN SIZE AND POSITION. 

Dilatation of the urethra may be produced by strictures, or by 

1 Virch. Arch., Bd. xlix., p. 348. 



THE URINARY APPARATUS. o71 

calculi or other bodies fixed in its lumen. The dilatations are fusi- 
form or sacculated in shape, and may reach the size of an oranj^e or 
be even larger. 

Strictures of the urethra are usually produced by inflammation ol 
its walls. 

The stricture may be temporary, produced by a diffuse inflamma- 
tory swelling of the mucous membrane, or by the raising of the re- 
laxed membrane into a fold or pocket. 

Perma7ient strictures are produced by structural changes in the 
walls of the urethra. 

1. The mucous membrane and submucous tissue are left hard 
and unyielding by the preceding inflammation. Subsequently the 
new fibrous tissue contracts and narrows the canal. 

2. Ulceration of the mucous membrane leaves cicatricial tissue, 
which contracts, and also produces adhesions and bands of fibrous 
tissue. 

3. There is fibrous induration of the corpus spongiosum and con- 
sequent constriction of the urethra. 

The most frequent position of strictures is at the junction of the 
membranous and spongy portions of the urethra, or close to this 
point. They also occur at the fossa navicularis and the meatus, but 
frequently in the prostatic portion. There may be one stricture or 
several. The consequences of stricture are dilatation of the urethra, 
the bladder, the ureters, and hydronephrosis ; inflammation and ul- 
ceration of the urethra behind the stricture, with perforation, infil- 
tration of urine, or the formation of fistulse. ^ 

The urethra may also be obstructed by folds of the mucous mem- 
brane ; by muscular valves at the neck of the bladder ; by wounds ; 
by polypi and swollen glands ; by new growths ; by changes in the 
prostate and perineum ; by calculi, mucus, blood, and echinococci 
coming from the bladder ; by foreign bodies introduced from with- 
out. 

Prolapse and inversion of the mucous membrane is seen in young 
girls and women in rare cases. There is a bluish-red swelling, from 
the size of a pea to that of a walnut, at the meatus. In the male 
invagination of the mucous membrane of the urethra has beiMi soon 
after injuries of the perineum 

WOUNDS — RUPTURE — PERFORATION. 

Wounds of the urethra are produced in many ways, but most 
connnonly by catheters and bougies. The wounds may cicatrize, or 

^ For litoratiire of stricture of urethra, and plates illustratinsr several forms, see 
article by Dlttel in Pitha and 15illrotirs "llandlnu'li der all^-. Chirurde." Hd. iii.. 
Abth. ;}. 



572 THE UEIXARY APPARATUS. 

there may be infiltration of urine or the formation of fistulse or false 
passages. 

Ruptures of the urethra are produced by severe contusions and 
by fracture of the j^elvic bones. Extravasations of blood and urme. 
and gangrenous inflammation of the surrounding soft i^arts. are the 
ordinary results. 

Ulceration and perforation of the urethra may lead to the forma- 
tion of fistulas, which open in various directions through the skin. 

IXFLA3IMATI0X. 

Catarrhal Urethritis may be simple and due to the action of 
chemical irritants, to the extension to the urethra of inflammation 
from other parts, and to unknown causes ; but it is most frequently 
due to the action of the gonorrhoeal poison. In its acute form it in- 
volves either a portion or the whole of the urethra. The mucous 
membrane is red, swollen, and covered Tvith muco-pus. The inflam- 
mation mav extend to the fibrous wall of the urethra, the corpora 
spongiosa and cavernosa. This may result in the formation of new 
connective tissue or of abscesses, especially near the fossa navicula- 
ris. The inflammation may also extend to the bladder, the glands 
of Cowper, the prostate, the spermatic cord, and the testicles. The 
ingTiinal glands also may be swollen and inflamed, and the hmiphatic 
vessels on the dorsum of the penis may be involved in the same pro- 
cess. 

Chronic inflammation of the urethra may exist for a long time 
with the production of a muco-purulent exudation, but -without the 
occurrence of marked structural lesions. In other cases it leads to 
ulceration, to fibrous induration of the wall of the canal, to indura- 
tion and swelling of the mucous follicles, to polypoid thickenings of 
the mucous membrane. 

The exudation in gonorrhoeal inflammation of the mucous mem- 
branes, not only of the urethra but also of the vagina and of the eye, 
constantly contains, in greater or less numbers, a form of micrococ- 
cus which is said by some observers — although this is denied by 
others — to present characteristic morphological characters. 

The micrococcus — called gonococcus — which is spheroidal or 
ovoidal in shape, usually occurs in pairs or in groups of four or more, 
and may be contained in the pus cells (Fig. 74) or lie on their sur- 
faces or free in the fluid. The pus cells sometimes contain very 
large numbers of the micrococci. 

The gonococcus may be stained by drying the exudation on a 
cover glass and using fuchsin or methylen blue. 

For details as to the biology of the gonococcus see page 165. 



THE URINARY APPARATUS. 573 

Croupous Inflammation is sometimes seen in children. Fibrin- 
ous casts of a small or large portion of the canal may be formed. 

Syphilitic Ulcers may be situated at the meatus or as far back 
as the fossa navicularis. They are apt to produce strictures. 

Tubercular Inflammation rarely occurs in the mucous mem- 
brane of the urethra in connection with tubercular inflammation of 
the bladder, prostate, or testicles. 

TUMORS. 

Aside from the polypoid outgrowths from the mucous membrane 
of the urethra as the result of chronic inflammation, fibrous polyps 
may occur congenitally, or polyps containing glandular structures 
or cysts rarely- occur. Carcinomcc may occur as a result of local 
extension from adjacent organs or metastasis from the bladder. 
Cysts may occur in the mucous membrane as a result of the dilata- 
tion of the mucous glands. Circumscribed masses of dilated veins 
occasionally occur in the urethra, forming the so-called urethral 
hcemorrhoids. 

The sinus pocularis may be dilated in children by the retention 
of its secretion, so as to form a tumor which may obstruct the exit 
of urine, cause hypertrophy of the bladder and dilatation of the 
ureters. 



THE OEaA:XS OF GEXERATIOX 



FEMALE GE:N"ERATIYE ORGAXS. 
THE VULVA. 

MALFORMATIONS. 

The external genitals may be entirely absent or imperfectly de- 
veloped. The fissure between the labia may be unformed, or the la- 
bia may grow together, with or without obstruction of the urethra. 
The clitoris and nymphse may be abnormally large, or the nymphse 
may be increased in number. The clitoris may be abnormally long, 
resembling a penis ; at the same time the vagina is narrow, the ute- 
rus small and undeveloped or malformed ; the ovaries small, some- 
times situated in the labia ; the mammae small, and the body of a 
masculine character. Such cases are sometimes called pseudo-her- 
maphrodites. The clitoris may be perforated by the urethra or may 
be cleft and apparently double. 

The hymen frequently exhibits various anomalies. It ma}^ be 
entirely absent. The opening may be very large or in unusual pla- 
ces ; there may be several openings ; the free edge may be beset 
with papillary projections ; there may be no opening at all.^ 

HEMORRHAGE, HYPEREMIA, ETC. 

Haimorrhage may take place from wounds or ulcers of the vulva, 
but the most important form of haemorrhage is that which occurs in 
the connective tissue of the labia majora. This is produced during 
labor or from external injury. One of the labia may be swollen and 
distended by the extravasated blood until it is as large as a child's 
head. The blood may be gradually absorbed, or it may decompose 
with suppuration or gangrene of the surrounding tissue. The puru- 

^ For description and illustrations of anomalies of the hymen, which may be use- 
ful for medico-legal purposes, see Gourtxfs ** Diseases of Uterus, Ovaries, Fallopian. 
Tubes," Trans, by McLaren, 1883, p. 90. 



THE ORGANS OF GENERATION. 575 

lent matter may escape through the skin and the patient recover, or 
the suppuration may extend into the pelvis and cause death. 

A varicose condition of the veins of the labia is not infrequent. 
CEdema may occur in acute form in pregnant and puerperal women, 
and may terminate in suppuration or gangrene. CEdema of the la- 
bia majora frequently accompanies disturbances of the venous cir- 
culation, as in certain heart and lung diseases ; or it may occur in 
chronic diffuse nephritis or other wasting diseases, or as a result of 
thrombosis or other disturbances of circulation in the uterine or peri- 
vaginal venous plexuses. This may be excessive, leading to the 
transudation of fluid through the skin, to the formation of vesicles, 
to superficial erosion, or even to gangrene. 

INFLAMMATION. 

The skin, mucous membrane, connective tissue, and glands of 
the vulva may be the seat of inflammation. Acute catarrh of the 
mucous membrane may be caused by a variety of irritating influ- 
ences, but is most frequently due to gonorrhoeal infection. The 
m\icous membrane is swollen and red and covered with a muco-pu- 
rulent exudation. The labia may be swollen, the glands of Bartho- 
lin are liable to be involved, and abscesses of the labia may be de- 
veloped. Chronic catarrhal inflammation may lead to superficial or 
deep ulceration of the mucous membrane, or to papillary outgrowths, 
or to thickening of the labia. Suppurative inflammation of the tis- 
sue of the labia may occur in connection with a similar process in 
neighboring parts. Erysipelatous inflammation of the skin of the 
vulva is frequent in young children and may cause death. In adults 
it is less common. Inflammation of the vulvo- vaginal glands may 
be acute and produce abscesses, or chronic and produce induration of 
the gland. 

Gangrene may follow erysipelatous inflammation, may occur after 
parturition, may accompany severe exhausting and infectious dis- 
eases, or may occur as an epidemic disease, especially among chil- 
dren. It may be the result of bruises or other injuries. In some 
forms, such as those known as noma and hospital (/aia/rene, the 
destruction of tissue proceeds with extreme rapidity. 

Herpes, eczema, lichen, prurigo, etc., may be found on the skin 
of the vulva. 

Syphilitic inflammation and ulceration are of frequent occurrence 
on the vulva, particularly on the mucous surfaces, and frequently 
lead to considerable destruction of tissue and cicatricial contractions. 

Simple Croupous Intlammafio)i may occur, with or without 
diphtheria and a similar lesion of the fauces or elsewhere, and is fre- 
quently associated with gangrene. 



o7(J THE ORGANS OF GENERATION. 

Lupus. — This form of inflammation, usually with more or less 
destructive ulceration, occasionally occurs in the vulva. 

TUMORS. 

Fibroma. — Circumscribed fibrous tumors are found in the con- 
nective tissue of the labia, mons veneris, perineum, clitoris, and 
entrance to the vagina. They may attain a large size, and, attached 
only by a pedicle, may hang far down between the legs. The skin 
is usually movable over the surface of these tumors. 

'Fibroma cliff usum (elephantiasis). — This usually involves the 
clitoris or the labia, or both, and may extend to surrounding parts 
of the skin. It consists essentially of a diffuse hypertrophy of the 
skin and subcutaneous tissue, mth or without involvement of the 
papillae and epidermis. The surface may be smooth or rough. 
Sometimes when the new growth is circumscribed, rough or smooth 
polypoid growths, often of large size, are formed. When the papillae 
ana epidermis are much involved, larger and smaller cauliflower-like 
excrescences may cover the hypertrophied parts and the surface be 
very rough and scaly. 

Papillomata. — These growths consist of hypertrophied papillae 
covered with thick layers of epithelium. They vary in size from 
that of a pea to that of an apple, and have a cauliflower appearance. 

Syphilitic Condylomata. — In one form, the so-called iniicoiis 
patch, there is an infiltration of the papillary layers of the skin or 
mucous membrane with variously shaped cells and fluid, so that the 
tissue has a gelatinous appearance. In other cases there is an 
hj^pertrophy of the papillae, so that larger and smaller wart-like ex- 
crescences are formed. This is called the pointed condyloma. 
Lipomata, fibro-myomata, and fibro-sarcomata are of occasional 
occurrence in the vulva. A few cases of melano-sarcoma are re- 
corded. Chondroma of the clitoris has been described. Carcinoma 
of the vulva may be primary, usually in the form of epithelioma of 
the clitoris or labia, or it may be secondary to cancer of the uterus, 
vagina, etc. 

Cysts are found in the connective tissue of the labia majora and 
minora. They are from the size of a pea to that of a child^s head. 
They may contain serum, colloid material, purulent or bloody fluid, 
or they may have the characters of dermoid cysts or atheroma cysts. 
Their origin is in many cases obscure. In some cases they are 
doubtless due to dilatation of lymph vessels. Cysts may be formed 
by a stoppage and filling with fluid of the canal of N'uck, or by a dila- 
tation of the ducts or acini of the vulvo-vaginal glands. 



THE ORGANS OF GENERATION. 577 



THE VAGINA. 



MALFORMATIONS. 

The vagina may be entirely absent, and the internal organs of 
generation also absent or imperfectly develox^ed. 

Either the upper or the lower portion of the canal may be absent 
while the remaining portion is present. 

The vagina may be closed by an imperforate hymen or by fibrous 
septa at any part of its canal. The canal may be abnormally small 
without being occluded. 

The vagina may be double, in connection with a double uterus ; 
or, while the uterus is normal, the vagina may be incompletely di- 
vided by a longitudinal septum. 

CHANGES IN SIZE AND POSITION. 

Dilatation of the vagina is produced by tumors, by the prolapsed 
uterus, and by the accumulation of blood and mucus behind con- 
strictions or obliterations of the canal. Lengthening of the vagina 
is produced by any cause which draws the uterus upward. JVa?^- 
roiving of the vagina is found as a senile change ; is produced by 
tumors and by ulceration of the wall of the canal. Extensive ulcers 
may even cause entire obliteration of the canal. 

Prolapse of the vagina occurs by itself, usually, as a result of 
thickening or laxity of its walls, or in connection with prolapse of 
the uterus. As an idiopathic process it usually takes place soon 
after parturition. A larger or smaller portion of the canal is in- 
verted and projects through the vulva. The entire circumference of 
the canal may be inverted and prolapsed, or only the anterior or pos- 
terior wall. The prolapse is at first small, but may afterward grad- 
ually increase in size and may drag down the uterus with it. In 
other cases prolapse of the uterus is the primary lesion, and the 
vagina is inverted b}^ the descent of that organ ; or the body of the 
uterus may retain its normal position, while an hypertrophy and 
lengthening of the cervix alone drag down the vagina. 

Hernia vesico- vaginal is — cystocele — may be either the cause or 
effect of a prolapse of the vagina and uterus. If the cystocele is the 
primary lesion, it begins as a small projection of tho wall oi' the Mad- 
der into the anterior part of the vagina. As the urine a^"^'ululllates 
in this sac it increases in size, projects through the vulva, draws 
down the vagina and the anterior lip of the cervix, and finally the 
entire uterus. If the cystocele is the secondary lesic^n, it is simply 
produced by the dragging-down of the posterior wall o\' the bladder 
bv the inverted vaii'iua. 



O.S. THE ORGANS OF GENERATION. 

Hernia intestiiio-vaginalis. — A portion of the intestines maybe- 
come fixed in Douglas' cul-de-sac between the rectum and the uterus. 
This portion of intestine gradually becomes larger, pushes forward 
the posterior wall of the vagina, inverts and fills up that canal, and 
finally projects through the vulva. It may drag mth it the pos- 
terior wall of the vagina and the uterus. 

Rectocele vaginalis. — A sac is formed by the projection of the 
anterior wall of the rectum and the posterior wall of the vagina. 
This lesion is of rare occurrence and does not reach a large size. 

When the vagina is prolapsed there is usually an inflammatory 
condition of the Hning membrane or a thickening of the epidermis. 

WOUNDS — PERFORATIONS. 

AVounds of the vagina are made by penetrating instruments, by 
forceps and other obstetrical Aveapons, and by the foetus during 
dehvery. Such woimds may heal, may give rise to large hsemor- 
rhages, may suppurate, may produce abscesses in the surrounding 
tissues, may leave fistulous openings into the vagina or maj' cause 
constriction or obliteration of its canal. 

Vesi CO- vaginal Fist nice are usually produced by injuries from 
instruments or from the foetus during delivery : less frequently by 
ulceration of the vagina, bladder, or adjacent connective tissue, or 
by abscess in the surrounding parts. The fistulse form an opening 
between either the bladder or the urethra and the vagina. They 
allow the urine to pass into the vagina. Spontaneous cure does not 
take place. 

Recto-vaginal Fistulce are formed in the same way as the last- 
mentioned. They allow the passage of ga s or faeces into the vagina. 
Thev sometimes heal spontaneouslv. 

INFLAMMATION. 

Catarrhal Inflarnrnation of the vaginal mucous membrane may 
be acute or chronic. It is most frequently caused by gonorrhoeal 
infection, but may be due to local irritation or depend upon general 
causes. It not infrequently occurs in the new-born. In the acute 
form the mucous membrane is swollen and frequently covered with 
a muco-purulent or a purulent exudation. In the chronic form the 
mucous membrane may be swollen, covered ^vith a jDurulent exuda- 
tion : there may be an exfoliation of epithelium, shallow or deep ero- 
sions, or ulcers. 

Sometimes large shreds or membranes are cast off from the va- 
gina which consist wholly of exfohated. flat epithelium (Fig. 267). 
In other cases the mucous membrane is thickened, dense, and some- 



THE ORGANS OF GENERATION. 579 

times pigmented, or it may be roughened, covered with papillae, or it 
may be relaxed and prolapsed. 

Croupous Inflammation may occur after parturition, in dysen- 
tery, in typhus and typhoid fever, diphtheria, scarlatina, measles, 
and other infectious diseases. The mucous membrane is swollen and 
covered with a grayish layer of fibrin and pus. The mucosa and 
submucosa may be infiltrated with fibrin and pus. The infiltrated 
portions of the mucosa and submucosa may die and become gangre- 
nous, and thus deep and extensive ulcers be formed. 

Suppurative Inflammation of the fibro-muscular coat of the 
vagina may occur after injuries or in pregnant and puerperal wo- 
men. Abscesses may be formed which penetrate into the lalna (jr 
into the pelvic connective tissue. In other cases the intense phleg- 




FiG. 267.— Vaginal Epithelium. 
A fragment from a large exfoliated mass. 

monous inflammation may lead to the death and casting-ott' of por- 
tions of the vaginal Avail, or even of the entire wall. 

Gangrene of the vagina may occur as a result of croupous or 
intense suppurative or syphilitic inflammation, or from unknown 
causes. In the form of noma it may be very extensive and rapidly 
destructive. 

Tubercidar and Syphilitic Inflammation, usually leading to 
more or less extensive ulceration, may occur in any ]>art of the 
vagina. Tubercular inflammation is secondary to tuberculosis of 
other parts. Syphilitic ulcers may heal, sometimes leaving marked 
cicatrices, and sometimes not. 

TUMORS. 

Fibroma, flbvo-mijoma, sai'coma, m/niina la-ricc/lularc, are of 



580 



THE ORGANS OF GENERATION. 



occasional occurrence in the vagina. Myoma striocellulare is of rare 
occurrence. 

Papillomata are of frequent occurrence as a result of chronic 
inflammation. Carcinoma of the vagina is usually secondary to 
cancer of the uterus. It may be primary as a circumscribed nodular 
tumor, or more frequently it occurs in a papillary and ulcerating 
form and often spreads to neighboring parts. 

Cysts. — These are not very common and may be small or as 
large as a hen's egg. They may be lined with flattened epithelium, 
and contain serous or viscid, dark-colored or transparent fluid. 

PARASITES. 

Among the animal parasites Oxyuris and Trichomonas vagina- 
lis are of occasional occurrence. Among the vegetable forms Oidium 
albicans, Leptothrix are occasionally seen, while micrococci and 
various other forms of bacteria are common. Staphylococcus and 
Streptococcus pyogenes have been found many times in the normal 
vagina. The pathogenic significance of the bacteria in the vagina 
is not yet established. 

THE UTERUS. 



MALFORMATIONS. 

The uterus, up to the third month of intra-uterine life, consists of 
two large cornua, which by the fusion of their lower ends form the 
uterus. 

The uterus, tubes, and vagina may be entirely absent, with or with- 
out absence of the external genitals. Or the uterus alone, or the 
upper part of the vagina also, may be absent. 

The uterus may be only rudimentary while the vagina is normal. 
It then appears as a flattened solid body \\4th solid cornua. Or there 
are two cornua joined at their lower extremities so as to form a small 
double uterus. Or the uterus is represented by a small sac, which 
may or may not communicate with the vagina. Or there is a A^ery 
small uterus, ^vith thin muscular walls and two large cornua. 

Only one of the cornua which should form the uterus may be 
developed while the other is arrested in its grov,^th. The uterus is 
then a long, cylindrical body, terminating above in one tube. On 
the side where the other horn should have been developed there is no 
tube, or only a rudimentary one. Both ovaries are usually present. 

The two cornua may be fully developed, but their lower ends 
remain separated and form a double uterus. An entire separation 
into two distinct uteri and vaginae is very rare. More f requenth' the 
uterus consists of one body, divided by a septum into two ca^dties. 



THE ORGANS OF GENERATION. 581 

There are then two cervical portions of the uterus projecting into 
a single vagina, or each into a separate vagina. Or there is only 
a single cervix. The septum in the uterus may be complete or only 
partial. 

We also find abnormal size of the uterus, abnormal flexions ; the 
cervix may be solid or may be closed by the vaginal mucous mem- 
brane. Or the cervix may have an abnormal form with a small 
opening or canal. ^ 

CHANGES IN SIZE. 

In the new-born infant the uterus is small, the body flattened, 
the cervix disproportionately large. During childhood the organ 
increases in size, but the body remains small in proportion to the 
cervix. At puberty the shape changes and the body becomes larger. 

At every menstruation the uterus is somewhat swollen and con- 
gested. After pregnancy it does not return to its virgin size, but re- 
mains somewhat larger. In old age it gradually becomes smaller : 
its walls are harder and more fibrous. 

Abnormal Sinallness of the uterus is sometimes found as an ar- 
rest of development. The uterus in adult life retains the size and 
shape of that of the infant. It may result, however, from chronic 
endometritis, from repeated pregnancies, from old age, or from 
chronic exhausting diseases. Its cavity may be smaller than nor- 
mal, or distended with mucus. Large myomata sometimes cause 
marked atrophy of the uterine wall. Atrophy of the vaginal portion 
of the uterus is sometimes observed after repeated pregnancies, some- 
times without known cause. Narrowing and obliteration of the 
cavity of the uterus and of the cervix are usually produced by chronic 
inflammation. 

Enlargement of the Uterus may be due to too early develop- 
ment. It is accompanied by abnormally early development of all the 
sexual organs and functions. The uterus mav bo enlarged in con- 
nection with heart disease, prolapse and abnormal flexions and ver- 
sions, chronic inflammations, repeated pregnancies, myomata, and 
accumulations of blood or mucus in the uterine ca\'ity. Enlarge- 
ment of the vaginal portion may be produced by the above causes, 
and is also found without knoAvn cause. One or both lips of the 
cervix may be uniformly increased in size, or they may be lobulated. 

Dilatation of the uterus is produced by arniinulations of bUxnl, 
mucus, or pus in consequence of narrowing or obliteration oi the cer- 
vix or vagina. The uterine walls may retain their normal thickness, 
be thickened or thinned. The most fre(|uent position of the stenosis 



' Illiistratious of various forms of inalforniatioii of tlu> corvix may bo found in the 
trauslation by McLaren of CouHija '* Diseases of the Uterus, Ovaries, etc.," 1883. 

51 



582 THE ORGANS OF GENERATION. 

is the OS internum. The retained contents after a time change in 
character, forming a thin, serous fluid — hydrometra — or they may 
be mixed with blood. The dilated uterus is not usually larger than 
an apple, but it sometimes reaches enormous dimensions. If both os 
internum and os externum are closed the cervical cavity may be also 
dilated and the uterus have an hour-glass shape. If the obstruction 
is in the vagina, the uterus and vagina may form a large, flask- 
shaped body, and the line of demarcation between cervix and vagina 
be lost. In some cases the dilatation is confined to the cervix. If 
the obstruction is not complete the retained fluid may escape into 
the vagina and afterward accumulate again. 

Accumulation of menstrual blood in the cavity of the uterus — 
hcematometra — is usually produced by congenital stenosis of the 
cervix or vagina. The dilated uterus may reach an enormous size. 
If the fluid is not evacuated by surgical interference there may be 
either rupture or ulcerative perforation of the uterus. The blood 
may escape into the abdominal cavity, or be shut in by adhesions, or 
perforate into the bladder or intestines. Sometimes the blood passes 
into the Fallopian tubes, dilates them, and escapes through their ab- 
dominal ends. 

CHANGES IN POSITION. 

The body of the uterus may become fixed in an abnormal position, 
while the situation of the cervix is unchanged. The body may be 
bent forward — anteflexion; backward — retroflexion ; or sideways 
— lateral flexion. The flexion may be slight, or so great that the 
neck and body form an acute angle. Anteflexion is the most com- 
mon variety, and that in which the flexion is greatest. Peritoneal 
adhesions, flaccidity of the uterine walls, particularly after delivery, 
atrophy of the walls, ovarian and other tumors, etc., are the usual 
causes of flexions. 

The Versions of the uterus consist in an abnormal inclination of 
the long axis of the organ to that of the vagina. The uterus may be 
inclined backward, forward, or to one side. 

Retroversion is very much the most common. The fundus uteri 
is directed backward and downward, the cervix forward and up- 
ward. This condition is found in various degrees ; in the highest the 
fundus lies in Douglas' cul-de-sac with the cervix upward, so that the 
axis of the uterus is parallel to that of the vagina, but in a direction 
nearly opposite to the normal one. Abnormal looseness of the ute- 
rine ligaments, abnormally large capacity of the pelvis, hypertrophy 
or tumors of the uterus, and pregnancy during the first four months, 
are some of the more common conditions under which this lesion 
occurs. 

Anteversion. — Inclination of the fundus forward and downward. 



THE ORGANS OP GENERATION. 583 

and of the cervix backward and upward, is not common and sel- 
dom reaches a high degree. It occurs under the same general ex- 
ternal conditions as anteflexion. 

Lateroversion is not very common as a simple lesion, but is not 
infrequently combined with other displacements. It may be pro- 
duced by congenital shortening of one of the broad ligaments, by ad- 
hesions, or by the pressure of tumors. 

The greater degrees of version may produce very grave lesions. 
The urethra and rectum may be compressed. Cystitis, perforation of 
the bladder, dilatation of the ureters and hydronephrosis, and fatal 
obstruction of the bowels may follow. If pregnancy exi.<[s abortion 
may take place, or the inverted uterus may be forced through the 
l^eritoneum and posterior wall of the vagina and project through 
the vulva. In the non-pregnant uterus pressure on the veins and 
consequent chronic inflammation of the organ may follow. 

Prolapsus Uteri consists of a descent of the uterus into the 
vagina. The uterus may be only slightly lowered or it may project 
at the vulva. In complete prolapse we find a tumor projecting 
through the vulva, partly covered by the distended vagina, and pre- 
senting the opening of the os externum near its centre. The blad- 
der and rectum may be drawn down with the vagina or may remain 
in place. The exposed cervix and vagina usually become inflamed 
and sometimes ulcerated, or the mucous membrane may become 
thickened. The lesion is frequently complicated by hypertrophy of 
the cervix. 

Gradual prolapse, which is most frequent, may be due to an in- 
creased weight of the uterus, as in pregnancy, inflammatory enlarge- 
ment, the presence of tumors, etc. ; or to some abnormal condition of 
the uterine supports. It is frequently caused by a vaginal cystocele 
or rectocele. Sudden prolapse is most apt to occur, in an enlarged 
uterus or one unduly heavy by reason of tumors connected with it. 
It is most common in subinvolution after parturition. 

Elevation of the uterus is produced by mechanical causes crowd 
ing or dragging it upward, as adhesions, tumors, etc. The vagina 
is drawn up and lengthened, and the vaginal portion of the cervix 
may be obliterated. 

Inversion of the uterus consists of an invagination of the fun- 
dus. The fundus may be invaginated in the body, the fundus and 
body in the cervix, or the entire organ in the vagina. It usually oc- 
curs when the uterine walls are relaxed, and is very frequently due 
to traction on the placenta during parturition. It may take place 
spontaneously after parturition. It may be produced by intra-uto- 
rine tumors. The mucous membrane of the inverted organ is fre- 
quently inflamed, particularly when the inversion is complete. 



1 



584 THE ORGANS OF GENERATION. 

Hernioe of the uterus are rare. Ventral hernice may occur dur- 
ing the latter months of pregnancy, the peritoneum, aponeuroses, 
and skin being forced outward to form a sac in which the uterus 
hes. Crural hernice are produced by the drawing-down of the ute- 
rus and ovaries into the sac of an intestinal hernia. Inguinal her- 
nia may be produced in the same way or be congenital. Ischiatic 
hernia has been seen. Pregnancy may occur in the uterus while 
situated in a crural or inguinal hernia. 

RUPTURE AND PERFORATION. 

Rupture of the unimpregnated uterus is rare. It may, however, 
occur when the uterine cavity is distended with blood or serum, or in 
connection with large myomata of the uterine walls. 

In the gravid uterus ruptures have been seen in nearly every 
month of pregTiancy, but most frequently toward the end. The rup- 
ture may be produced by thinning of the uterine wall by tumors, or 
by violent contusions, or as the result of cicatricial contraction of 
the OS. 

The act of parturition is the most frequent cause. Malpositions 
of the foetus, narrowing of the pelvis, protracted labor, thinning of 
the uterine wall from tumors, forcible use of the forceps and other 
instruments, are the ordinary causes. The rupture may be in the 
body of the uterus or the cervix, or both ; it may be large or small ; 
it may extend completely or only partly through the uterine wall. 
The consequences of partial rupture are hsemorrhage, gangrenous 
inflammation of the edges of the rupture, peritonitis, and usually 
death. In rare cases the rupture cicatrizes and the patient recov- 
ers. Complete rupture usually causes death in a short tirae. The 
foetus escapes partly or completely into the abdominal cavity. If 
the patient survives the immediate shock, fatal peritonitis soon en- 
sues. In rare cases the foetus is shut in by adhesions and the pa- 
tient survives. 

Perforations of the uterus may be produced by carcinoma, by 
abscesses in its neighborhood, and hj ovarian cysts. 

HTPER.EMIA— UTERINE AND PERI-UTERINE HEMORRHAGE. 

Hyperoemia. — Aside from the active menstrual hypersemia, the 
uterus may be hypersemic in acute and chronic inflammation, as a re- 
sult of displacement of the organ, and in certain forms of heart dis- 
ease. The organ is usually enlarged, the mucous membrane swol- 
len, and the veins more or less e^ddently dilated. 

Hcemorrhage. — Effusion of blood into the cavity of the uterus 
occurs normally at the menstrual periods. For the abnormalities to 
which, this function is subject we refer to works on gynsecology. 



THE ORGANS OF GENERATION. 585 

Effusions of blood at other than the menstrual periods may be caused 
by mechanical hyperaemia, by haemorrhoids, by acute hypersemia, 
by intra-uterine polypi and other tumors, by acute and chronic in- 
flammation, by typhus fever, scurvy, etc. , by ulcerating carcinoma, 
by abortions and miscarriages. 

A peculiar form of hsemorrhage is the polypoid hsematoma, or 
fibrinous polypus of the uterus. It occurs after parturition and after 
abortions. The portion of the uterine wall where the placenta was 
attached, with or without a portion of retained placenta, forms the 
point of attachment of the pedicle of the polypus. We find a large, 
polypoid, bloody mass firmly attached by a pedicle to the uterine 
wall. The uterus enlarges with the growth of the polypus, the cer- 
vix is dilated, and the thrombus projects into and may even fill up 
the vagina. The formation of such a thrombus is accompanied by 
repeated haemorrhages. 

Haemorrhage . in the substance of the uterus occurs in old age. 
The mucous membrane and uterine wall are infiltrated with blood, 
and there is some blood in the uterine cavity. 

Peri-uterine or Retro-uterine Hcematocele consists in an accu- 
mulation of blood around the uterus or in Douglas^ cul-de-sac. It 
may consist of blood extravasated into the abdominal cavity, which 
settles into the pelvis ; or, in consequence of local hypersemia, there 
may be repeated extravasations of blood. In the latter case the local 
peritonitis may produce false membranes, between the layers of 
which haemorrhages take place. A similar condition rarely occurs 
in the male. The haemorrhagic mass may become encapsulated, or 
may soften or suppurate and perforate into the rectum or vagina, or 
may be absorbed. A form of extraperitoneal haematocele is de- 
scribed in which the blood lies between the folds of the broad liga- 
ment. The extravasation may proceed from haemorrhage of any of 
the abdominal viscera or rupture of aneurisms ; from vascular new- 
formed false membranes ; from rupture of the varicose veins of the 
broad ligaments ; from rupture of haemorrhagic cysts of the ovaries ; 
from the Fallopian tubes in tubal pregnancy or in haematometra ; or 
from general causes, such as scurvy, purpura, etc. In S3me cases 
the extravasation begins at a menstrual period, and increases at the 
succeeding periods. 

Ante-uterine Hcematocele is of occasional occurrence, either in 
connection with the retro-uterine form or when the posterior oul-do- 
sac is obliterated. 

INFLAMMATION. 

/. Inflamniatioli of the LDiinipregiiafciI rtt'ni,s. 
Acute C(ytarrhal Eudonictritis. — In this disease, which in its 



586 



THE ORGANS OF GENERATION. 



lighter grades may leave but little alteration after death, the mucous 
membrane is swollen, hyperaemic, and sometimes the seat of punc- 
tate h8emorrhageS4 The epithelium may desquamate, and the mu- 
cosa contain an undue quantity ^of small spheroidal cells. The sur- 
face is more or less thickly covered with muco-purulent exudation. 
In severe cases shreds of mucous membrane may be exfoliated. The 
lesion is usually most marked in the mucous membrane of the body. 







Fig, 268.— Chronic Endometeitis with the Formation of a Polypoid Outgrowth from the 

Mucous Membrane. 

but may involve the cervix at the same time, or the cervix alone. 
The body of the uterus may be swollen and hyperaemic. In dys- 
menorrhoea memhranacea there may be an expulsion, with more or 
less blood, of membranous masses consisting of fibrin mingled with 
blood and pus cells, or consisting of exfoliated superficial layers of 
epithelium. This exfoliated epithelium is frequently much flattened 
so as to considerably resemble the vaginal epithelium. When the 
shreds are large the openings of the uterine glands may be seen as 
perforations. Acute catarrhal inflammation of the uterus may be 



THE ORGANS OF GENERATION. 



587 



due to injury, exposure during menstruation, the gonorrhoeal infec- 
tion, local infection with other bacteria, or it may accompany the 
general acute infectious diseases. 

Chronic Endometritis. — This may be a continuation of an acute 
inflammation or begin as a chronic disease. In some of the lesser 
degrees of inflammation we find but slight changes after death. 
The mucous membrane, on the other hand, may be swollen, hyperae- 
mic, and covered with muco-purulent exudation. In other cases 
there is more or less well-marked thickening of the mucous mem- 
brane, which may present a smooth or a rough papillary surface or 
polypoid outgrowths (Fig. 268). Owing to the hypertrophy of the 







Fig. 269.— Adenomatous H^epbrplasia of the Uterine Mttcous Membrane. 
This section is from a large polypoid outgrowth which protruded from the cervix uteri 

uterine glands in this condition, these papillary outgrowths, which 
are not infrequently scraped off by the surgeon, often present the 
appearance of adenomata. This condition is called *" adenomatous 
hyperplasia of the uterine mucous membrane " (see Fig. 209). Some- 
times a thick layer of new-formed, very vascular tissue develops over 
the surface of the mucous membrane, largely covering in the uterine 
glands (Fig. 270). From the decomposition of extra vasated blood in 
the mucous membrane the latter may be mottled with brown or 
black. The glandular elements of the mucosa may be partially or 
almost entirely destroyed. The papilliB of the cervix may be liyjxn-- 
trophied, tlie mucous follicles swollen and their outlets obstructed, 
leading to the formation of the so-called ovula ISTabothi. The uto- 



588 



THE ORGANS OF GENERATION. 



rine wall becomes flaccid and atrophied, or it may be hypertrophied, 
especially in the cervical portion. Ulceration of the mucous mem- 
brane, especially of the cervix, may occur. Contraction or oblitera- 
tion of the cervical canal may occur. The inflammation may extend 
to the Fallopian tubes or to the vagina. 

Chronic endometritis may exist at any age, but is most common 
after puberty, and is produced by a great variety of causes. It may 
occur in ill-nourished persons or in those suffering from exhausting 
diseases. It may be due to displacements and tumors of the uterus, 
subinvolution, injuries, etc. 




'yyaifisr^. 



Fig. 270.— Chronic Endometritis with the Formation of a Thick Layer of New-formed, very 
Vascular Tissue over the Surface of the Mucous Membrane. 

a, uterine muscle tissue; b, mucous membrane of uterus; c, new -formed vascular tissue. 

Croupous Endometritis. — This form of inflammation is not very 
common. It occasionally occurs in the puerperal uterus, in acute 
infectious diseases, cholera, typhoid fever, the exanthemata, etc. 
The disease sometimes involves the vulva, vagina, and Fallopian 
tubes. It may co-exist with croupous inflammation of the colon. 

Tubercular Endometritis. — This usually occurs as part of tuber- 
cular inflammation of the genito-urinary tract. We find a part or 
the whole of the cavity of the uterus lined with a rough, yellowish 
or gray, cheesy mass, which may deeply involve the muscular walls 
of the organ. At the edges of the ulcerating cheesy areas we may 



THE ORGANS OF GENERATION. 589 

find well-defined miliary tubercles, or we may find tubercles scattered 
through the otherwise intact mucosa. The lesions resemble those of 
tubercular nephritis. 

Syphilitic Endometritis. — The results of this infection are 
usually confined to the cervical portion, and consist of shallow or 
deep ulcerations and condylomata of the mucous membrane ; or there 
may be a diffuse thickening of the mucosa. 

Acute Metritis is usually the result of acute catarrhal endome- 
tritis. The organ is swollen, succulent, congested ; the mucous 
membrane covered with muco-pus ; the peritoneal coat congested. 
There may be smaJl extravasations of blood in the wall or cavity of 
the uterus. The inflammation, in rare cases, becomes suppurative, 
and abscesses are formed in the uterine wall ; these may perforate 
into the peritoneal cavity or into the rectum. 

Chronic Metritis is the result of an acute metritis or accompanies 
acute or chronic endometritis, and is dependent upon the same con- 
ditions : subinvolution, displacements, tumors, active irritants, etc. 
The uterus is enlarged, the wall congested, thickened, and soft. Or, 
owing to the new formation of connective tissue, hard and dense. 
The lesion may be most marked in the body or in the cervical portion. 

Perimetritis. — The peritoneal coat of the uterus may be inflamed, 
with the production of membranous adhesions or of pus. The 
adhesions may be small or very extensive, and, owing to their con- 
tractions, may cause various distortions and displacements of the 
pelvic organs. The inflammation is usually an accompaniment of 
chronic metritis and endometritis. In prostitutes such adhesions 
are of very common occurrence. 

Parametritis. — The connective tissue about the uterus, between 
that organ and the reflexions of the peritoneum, may be the seat of 
suppurative inflammation. It most frequently causes the death of 
the patient, but may result in the formation of dense connective 
tissue about the uterus. 

II. Inflammation of the Pregnant Uterus. 

The forms of inflammation which have just been described may 
attack the pregnant uterus. Catarrhal endometritis may produce 
effusion of serum, extravasations of blood, and abortions. Metritis 
may lead to softening of the uterine wall, so that rupture takes place 
during labor. Perimetritis and parametritis produce adhesions and 
abscesses about the uterus. 

Picer'peral Inflammation. 

For a week or more after delivery we find the inner surface of 
the still dilated uterus rougli, especially at the insertion of the pla- 
53 



590 



THE ORGANS OF GENERATION. 



centa, and covered with blackened, gangrenous-looking shreds of 
blood, mucous membrane, and placenta. This condition is not to be 
mistaken for inflammation. 

As a result of some injury to the uterus or vagina during or af- 
ter delivery, and the action of some infectious material which may 
gain access to the tissues, the puerperal uterus is liable to become 
the seat of a series of severe and often destructive inflammatory and 
"necrotic changes. These may be confined to the uterus ; they may 
induce serious alterations in surrounding parts ; they may lead to an 
involvement of the peritoneum, or to pyaemia and its accompanying 







Fig. 271,— Uterine Phlebitis following Delivery with Retained Placenta, 
Death nine days after delivery. Micrococci in the walls of the inflamed veins stained violet. 



lesions in the most distant parts of the body. In one series of cases 
a more or less extensive gangrenous inflammation of the mucous 
membrane and the underhung parts may lead to the casting-off of 
larger and smaller shreds of necrotic tissue and the formation of 
deep and spreading ulcers, which may be accompanied by severe 
parametritis and fatal peritonitis. This condition may be due to in- 
jury or to the presence of decomposing portions of retained placenta. 
In other cases the inflammation has a croupous character, which may 
affect the vagina and lead to necrosis and gangrene, ulceration, and 
peritonitis. In connection with either of the a.bove forms of inflam- 
mation, or without them, there may be thrombosis of the uterine 
sinuses, purulent inflammation of the veins, suppuration and ab- 



THE ORGANS OF GENERATION. 591 

scess in the uterine wall, suppurative inflammation of the ovaries 
and tubes, and, owing to the generalization of the infectious mate- 
rial, metastatic abscesses in the lungs, spleen, kidneys, etc. Or 
acute pleurisy, ulcerative endocarditis, purulent inflammation of the 
joints, hyperplastic swelling of the spleen and lymph nodes, may fur- 
nish characteristic features of the presence of an acute infectious dis- 
ease. In some cases which rapidly pass to a fatal termination the 
local lesions may be but slightly marked, and general alterations 
characteristic of pyaemia, such as metastatic abscesses, etc., be en- 
tirely wanting. Life seems to be overcome by an acute septic in- 
toxication. 

Micrococci are very constantly present in the exudation, in the 
lymph vessels, veins, and inflamed tissue of the uterus (see Fig. 
271) ; often in enormous quantities in the peritoneal exudation and 
in the metastatic inflammatory foci. There is good reason for be- 
lieving that the destructive local processes are due, in the majority 
of cases, to the presence of the Streptococcus pyogenes, and that the 
general infection in this, as in other forms of septicaemia and pyae- 
mia, is dependent upon the same cause (see Septicssmia). 

ULCERATION AND DEGENERATION. 

Catarrhal, tubercular, and syphilitic ulceration have been 
mentioned above. 

Phagedenic or Corroding Ulcer. — This rare form of ulceration 
usually occurs in old age, without assignable cause. It begins in the 
cervix and gradually extends until it may destroy the greater part 
of the uterus or even invade the bladder and rectum. The ulcer is 
of irregular form ; its base is rough and blackish, its walls indu- 
rated. It should not be confounded with carcinomatous ulcer, which 
it considerably resembles. 

Fatty Degeneration. — This may occur in connection with in- 
flammatory changes-, in acute infectious diseases, and in phosphorus 
poisoning. 

Amyloid Degeneration iwthe wtQvw^ is of rare occurrence. It 
may affect the muscle fibres or the walls of the blood vessels. 

TUMORS. 

Fibromata. — Dense nodular fibromata of the uterus are exceed- 
ingly rare, the so-called fibromata being in most cases myoma ta or 
fibro-myomata. Fibroma papillare, on the other hand, is a com- 
mon iovxw of growth from the mucous membrane. It consists of a 
more or less vascular connective-tissue stroma covered with epithe- 
lium. The surface may be smooth or villous. It may contain 
very numerous gland follicles, and thou approaches the type of 



592 THE ORGANS OF GENERATION. 

adenoma, or even carcinoma. The stroma may be loose and succu- 
lent, and resemble mucous tissue, forming the so-called mucous 
polypi J and these again may contain glandular structures. In any 
of these forms the blood vessels may be abundant and dilated, form- 
ing telangiectatic or cavernous polypi. The adenomatous polypi may 
become cystic from the dilatation of the gland follicles. 

Polypi of the uterus may be multiple or single, small or large. 
J^umerous smaller and larger papillary outgrowths from the mucous 
membrane may occur in chronic endometritis. Single polypi may 
grow from the mucosa of the body of the uterus or from the cervix, 
and hang by a long pedicle down into the vagina. 

The large number of glandular structures in many of these chro- 
nic inflammatory, papillary, and polypoid outgrowths (Figs. 265 
and 269) often justifies the name of adenomatous hyperplasia of the 
mucous membrane or of adenomatous papillomata or polyps. 

Syphilitic papillary growths in the form of pointed condylomata 
may form finely papillary, wart-like excrescences of variable size, 
particularly on the cervix. 

Myomata. — These tumors, whose characteristic structural ele- 
ments are smooth muscle cells (see Fig. 121), are the most common of 
uterine tumors and are frequently of no special practical importance, 
but are sometimes of very serious import. They are especially com- 
mon in negroes. They are most frequently composed of both mus- 
cular and fibrous tissue — fibro-myomata — but the relative amount 
of the two kinds of tissue is subject to great variation. They are 
most apt to occur after puberty, and usually in advanced life. They 
may be single or multiple, small or of enormous size ; are usually 
sharply circumscribed, whitish or pink, dense and hard, or some- 
times soft, and present on section interlacing bands or irregular 
masses of glistening tissue. Their favorite situation is in connection 
with the body of the uterus, but they raay occur in the cervix or 
in the folds of the broad ligaments. According to their position 
we may distinguish subserous, submucous, and intraparietal forms. 
The subserous myomata grow from the outer muscular layers of 
the uterus in the f orixi of little nodules. As they increase in size 
they may become separated from the uterine wall and remain at- 
tached only by a narrow pedicle or by a little connective tissue. 
They may work their way between the folds of the broad ligament 
until they are at some distance from their point of origin. Some 
authors mention cases in which the tumors became entirely detached 
from the uterus and were free in the abdominal cavity. In some 
cases the tumors excite inflammation of the adjacent peritoneum, 
leading to the formation of adhesions or of collections of pus. Cases 
are recorded in which, omng to the atrophy of the pedicle, subserous 



rjQ 



THE ORGANS OF GENERATION. 0^:3 

myomata have become completely detached from the uterus and 
were held in place and nourished by peritoneal adhesions. In other 
cases the tumor reaches a large size, bat remains firmly attached to 
the uterus. This organ may then be drawn upward, the cervix and 
vagina being elongated and narrowed. The traction may be so great 
that the body of the uterus is entirely separated from the cervix. 
The bladder may also be drawn upward, producing incontinence of 
urine and cystitis. Subserous myomata are very often multiple and 
frequently attain great size. 

The submucous myomata grow from the inner muscular layers 
of the uterine wall. They commence as rounded nodules which lift 
up the mucous membrane. The usual position is the fundus uteri. 
They rarely occur in the cervix. As the tumors increase in size they 
project into the uterine cavity. They then remain continuous with 
the uterine wall over a large area, or are attached by -a large or 
small pedicle. They are usually well supplied with vessels. The 
uterus dilates with the growth of the tumor, and its walls may be 
also thickened. The tumor may reach such a size as to entirely fill 
the cavity of the dilated uterus and project through the cervix into 
the vagina. 

The submucous myomata are usually single, although there may 
be at the same time subserous and intraparietal tumors. They are 
frequently soft. If they are of large size and polypoid in form, they 
may project through the cervix and drag down the fundus of the 
uterus, producing inversion. The mucous membrane covering them 
may be atrophied or hypersemic, with dilated blood vessels, and may 
thus give rise to severe and repeated hgemorrhages. Haemorrhage 
may occur in the substance of these tumors. Inflammation, suppu- 
ration, and gangrene may also occur. The surface may be ulcerated. 
In some cases the pedicle of the tumor is destroyed and it is sponta- 
neously expelled. 

The intraparietal myomata grow in the substance of the uterine 
wall, but, if they attain a large size, project beneath the serous or 
the mucous coat. They are found in every part of the uterus, but 
are most frequent in the posterior wall. 

The shape of the uterus is altered in a great variety of ways by 
the presence of these tumors ; its cavity is narrowed, dilated, or 
misshapen ; it undergoes flexion and version in every direction. The 
tumors may sink downward and become attached to the pc^sterior 
wall of the vagina, looking as if they grew from it. They may, 
without the formation of a pedicle, project into the cavity of the 
uterus, fill it up, and project through the cervix. The uterus is 
dilated, its wall hypertrophied or atrc^phied. 

The tumors themselves may undergo a. variety of secondary altera- 



594 THE ORGANS OF GENERATION. 

tions. The muscle fibres may undergo fatty degeneration, and the 
tumor diminish in size, or may even undergo, it is said, entire destruc- 
tion and atrophy. Calcification may occur, converting a part or the 
whole of the tumor into a stony mass. The intraparietal and sub- 
mucous myomata may give rise to profuse haemorrhages ; thay may 
suppurate and become gangrenous. 

Sometimes the tumors or circumscribed portions of them are very 
•vascular, constituting the telangiectatic or cavernous variety. 
These tumors, which possess some of the characters of erectile tissue, 
may suddenly change in size from a variation in the amount of blood 
which they contain. 

A very important change which is sometimes found in these 
tumors is the development of cysts in their interior (fibro-cystic tu- 
mors). This sometimes takes place in those tumors which grow out- 
ward beneath the peritoneal coat. We find one or more cavities 
communicating with each other, with rough, trabeculated walls. 
The appearance is more that of cavities than of cysts. There may 
be a number of smaller cavities, or they may fuse to form one large 
one. The fluid contained in the cavities is like synovia, or is mixed 
with blood. These cystic myomata may reach an immense size and 
fill the abdominal cavity. The diagnosis, during life, between them 
and ovarian cysts is often very difficult, and they have frequently 
been the subjects of fatal operations. 

In the cervix uteri myomata are rare. They may grow as polypi 
beneath the mucous coat, or produce enlargement of the anterior or 
posterior lips, or may grow outward into the abdominal cavity. 

Combinations of myoma and sarcoma sometimes occur — myo- 
sarcoma. 

Sarcomata may occur as primary tumors in the mucous mem- 
brane of the uterus, either in the form of a diffuse infiltration or as a 
circumscribed nodular or polypoid mass. They frequently involve 
the muscular wall, are liable to haemorrhage and gangrene, and, 
particularly in the diffuse form, are liable to recur after removal. 
They may consist largely of spindle or spheroidal cells, or both. It 
is said that sarcoma of the uterus is more liable to occur at an ad- 
vanced age than at an early period, as is the rule with sarcomata of 
other organs. 

Angioma. — A small, cavernous angioma of the wall of the uterus 
has been described. 

Adenoma. — Between a simple adenomatous hyperplasia of the 
mucous membrane of the uterus, on the one hand (see Figs. 268 and 
269), and carcinoma on the other, there is no absolutely sharp mor- 
phological distinction. But there is a consider.able group of growths, 
to which the name adenoma is properly applied, which lie on the 



THE ORGANS OF GENERATION. 



595 



border zone between the distinctly benign and the definitely malig- 
nant new epithelial tissue growths. 

Many epithelial cell growths of the uterus, while adenomatous in 
structure, are so distinctly malignant, and are so liable to develop that 
structural lawlessness characteristic of carcinoma, that it has seemed 
wise to many observers to avoid the name adenoma altogether and 
class all the epithelial tumors of the uterus among the carcinomata. 
Others, recognizing the benign character of many of the epithelial 
tumors of the uterus, have adopted a sharp distinction between be- 
nign and malignant adenoma. 

It seems to the writer wise to preserve here, as elsewhere in the 
body, the morphological distinction between adenoma and carcinoma. 







Fig. 272.— Adenoma of the Uterus. 
Showing papillary outgrowths and commencing infiltration of the submucous tissue. 

But in doing this it should always be borne in mind that the adeno- 
mata of the uterus, as those of the gastro-intestinal canal, may not 
only be extremel}^ malignant as adenomata, but that the more benign 
forms are extremely prone to develop, both in structure and malig- 
nancy, into carcinomata. In fact, in many cases we can only express 
the peculiarities of structure in these tumors by calling them adeno- 
carcinoma. 

The adenomata of the uterus may begin in a simple hyperplasia 
of the mucous membrane, in which glaiidular development is pre- 
ponderant. This new glandular growth is most commonly in the 
form of irregular, often dilated follicular structure with a well- 
marked lumen lined with cylindrical or caboidal cells. The new 



596 



THE ORGANS pF GENERATION. 



growth may project from the inner surface of the uterus m the form 
of papillary masses, or it may infiltrate the submucous tissues. Or 
growth in both directions may occur at once. (See Figs. 272 and 273.) 

The topographical features and clinical stories of many adeno- 
mata of the uterus are identical with those of the infiltrating and ul- 
cerating carcinomata. 

Carcinoma. — The carcinomata of the uterus commence most 
frequently in the cervix and portio vaginalis, and the most common 
form is the epithelioma. The growth of epitheliomata of the cervix 
uteri proceeds under three tolerably distinct forms, which, however, 
frequently merge into one another. 




Fig. 273.— Adenoma of the Uterus. 
Small portion of specimen shown in Fig. 272, more highly magnified. 



1. The Flat, Ulcerating Epithelioma.— This form of cancer 
commences as a somewhat elevated, flat induration of the superfi- 
cial layers of the cervix, sometimes circumscribed, sometimes diffuse. 
This induration is due to the growth of plugs and irregular masses 
of epithelial cells into the underlying tissue. Ulceration usually 
commences early and may proceed slowly or rapidly. The edges of 
the ulcer are irregular, indurated, and somewhat elevated. The 
ulceration of the new-formed cancerous tissue at the edges is usuallj^ 
progressive, so that the vaginal portion of the cervix, the cervical 



THE ORGANS OF GENERATION. 



o97 



canal, the vagina, and even the bladder and rectum may be in- 
volved. More or less extensive haemorrhages and necrosis of the 
base of the ulcer are liable to occur. The entire cervix may be de- 
stroyed. 

2. In another class of cases the carcinomatous growth develops 
under the form of papillary or fungous excrescences, which may 
form larger or smaller ma-sses composed of ejjitheliomatous tissue. 
Hand-in-hand with this projecting growth there may occur an epi- 
thelial infiltration of the underlying tissue of the cervix. These 








Fig. 274.— Carcinoma op the Cervix Uteri (Ulcerating). 



growths are often quite vascular and may give rise to severe hi^m- 
orrhages. They may ulcerate and thus produce great destruction of 
tissue. 

3. In still another class of cases there is a more or less deep infil- 
tration of the submucous tissue, either diffuse or in circumscribed 
nodules, with epithelial cell masses. We find at first, in the vagi- 
nal portion of the cervix, in the submucous connective tissue, either 
nodules or a general infiltration of a whitish new growth. The cer- 
Adx then appears large and hard. Very soon the mucous membrane 
53 



598 



THE ORGANS OF GENERATION. 



over the new growth degenerates and falls off ; the superficial la}'- 
ers of the new growth undergo the same changes. After this the 
formation of the new growth and its ulceration go on simultane- 
ously, producing first an infiltration and then destruction of the cer- 
vix, and often of a part of the body of the uterus. The growth fre- 
quently extends to the vagina, the bladder, and the rectum with the 
same destructive character, so that we often find the cervix and up- 
per part of the vagina destroyed, and in their place a large cavity 




-^^S, 



>M?oA^-j 









.fMfJ^^.y^ 



Fig. 275.— Carcinoma (Epithelioma) of the Uterus. 
Showing ramifying epithelial cell masses. 

with ragged, gangrenous, cancerous walls (Fig. 274). Less fre- 
quently the pelvic bones are invaded in the same way. !N"ot infre- 
quently the ureters are surrounded and compressed by the new 
growth, so that they become dilated. The dilatation may extend to 
the pelves and calyces of the kidneys. The new growth may begin 
in the cervix and extend uniformly over the internal surface of the 
cervix and of the body of the uterus. The entire uterus is converted 
into a large sac, of which the walls are infiltrated with the new 



THE ORGANS OF GENERATION. 590 

growth, while the internal surface is ulcerating and gangrenous. In 
some cases there is a considerable formation of new, dense connec- 
tive tissue, so that the growth has a scirrhous form. 

In rare cases the growth begins in the upper part of the cervix 
or in the body of the uterus, while the lower part of the cervix is not 
involved. In all of these cases the epithelial cells of the new growth 
follow more or less closely the type of the epithelial cells of the part 
from which they spring (Fig. 275). 

In still another class of cases, in which the new growth may be 
in the form of nodules, or diffuse infiltrations, or polypoid masses, or 
may present more or less extensive alterations, the cells are irregu- 
lar, polyhedral in shape, the tumor belonging to the class of glan- 
dular or medullary carcinomata. These also usually commence in 
the cervix, and, according to the views of many writers, probably 
in the mucous glands. 

In rare cases the entire wall of the uterus is infiltrated with the 
new growth and the organ is much enlarged. Colloid carcinoma 
sometimes occurs, but is rare. 

While we may for convenience recognize the above types of car- 
cinoma of the uterus, it should be borne in mind, as above stated, 
that they are not apt to be perfectly distinct, and some of them may 
merge into one another or exist simultaneously. Exudative inflam- 
mation is of frequent occurrence in these as in other tumors of the 
uterus (see Fig. 133). 

As a result of the ulceration of these various forms of carcinoma 
recto-vaginal fistuloe may be formed ; the lumbar lymph nodes may 
be involved, and metastases in distant organs are occasionally 
though not frequently formed. Frequent and profuse haemorrhages, 
gangrenous destruction of tissue, the absorption of deleterious mate- 
rials, etc., are apt to lead to the development of a more or less pro- 
found anaemia and cachexia. 

PARASITES AND CYSTS. 

Various forms of bacteria are of frequent occurrence in the 
cavity of the uterus when the organ is diseased. The presence of 
some is significant, and of others not. Echiiiococcus has been found 
in the body and neck of the uterus, and may rupture into the peri- 
toneal cavity or into the vagina. 

Cysts. — Aside from the cysts which develop in tumors of the 
uterus, in the cervix uteri the mucous follicles are frequonth' so di- 
lated as to form cvsts filled with a Q'olatinous material and more vn* 
less epithelium. These cysts may bo large or small, and are fre- 
quently called ovula Nahothi. Sometimes there is an intiammatory 
growth of new connective tissue about these cysts. In other oases 



600 THE ORGANS OF GENERATION. 

the cysts may project from the mucous membrane in the form of 
polypi. Similar changes are infrequently found in the body of the 
uterus from the dilatation of occluded uterine glands. Dermoid 
cysts are rarely found in the walls of the uterus. 

THE OVARIES. 
MALFORMATIONS. 

One or both ovaries may be absent, the other organs of generation 
being also absent or undeveloped. Or the ovaries may be only par- 
tially developed. Absence or arrest of development of one ovary is 
sometimes met with in otherwise well-formed individuals. It is 
sometimes accompanied by a low position of the kidney on the same- 
side. The ovaries may pass into the inguinal canal or into the labia 
majora, and remain fixed there through life. Less frequently they 
are found in the crural canal or the foramen ovale. 

CHANGES IN SIZE. 

The ovaries may become larger than normal by chronic inflam- 
mation, by the formation of cysts and tumors. They may become 
atrophied in old age, the Graafian follicles disappearing and the 
organ shrivelling into a small, irregular, fibrous body. Atrophy 
may be produced by ascites, by chronic inflammation, or from un- 
known causes. As the result of the maturing and rupture of the 
Graafian follicles, with and without pregnancy, the surface of the 
ovary, which before puberty is smooth, may become roughened by 
irregular cicatricial depressions. 

CHANGES IN POSITION. 

In adult life the ovaries may pass as liernise into the inguinal or 
crural canal, the foramen ovale, or the umbilicus. 

The position of the ovaries in the abdomen may be changed by 
the pressure of tumors, the traction of false membranes, etc. It may 
occur in enlarged ovaries or in those of normal size, and by the com- 
pression of the veins may lead to congestion and chronic inflammation 
of the organ. 

HYPEREMIA AND HAEMORRHAGE. 

Aside from the normal hypersemia of the ovaries during menstru- 
ation, the vessels may be congested in inflammation, in displace- 
ments with interference Avith the venous circulation, in certain 
diseases of the heart, etc. , and may then be followed by chronic 
inflammation. 

The .menstrual periods are accompanied by the effusion of blood 



THE ORGANS OF GENERATION. 601 

into a Graafian follicle. IN'ormally the amount of blood is small, 
becomes solid, is decolorized and then gradually absorbed. Some- 
times the effusion of blood is much greater ; the follicle filled with 
blood is as large as a pigeon^s egg. The blood may remain in the 
follicle and be absorbed, and replaced by a serous fluid, or it may 
rupture it and escape into the peritoneal cavity. Death may ensue 
from the haemorrhage, or the blood may collect in Douglas' cul-de-sac 
and be enclosed in false membranes. Heemorrhages also occur in 
follicles which have become cystic. Interstitial haemorrhage in the 
ovary sometimes occurs without known cause. 

INFLAMMATION (OOPHORITIS). 

Acute Inflammation of the ovaries occurs most frequently in the 
puerperal condition, either as part of a general peritonitis or as a 
primary affection. 

With puerperal peritonitis both ovaries are usually inflamed ; 
they are swollen, congested, soft, infiltrated with serum or pus, or 
gangrenous. The inflammation may attack principally the capsule, 
the stroma, or the follicles. Inflammation of the capsule results in 
adhesions and collections of pus, shut in by false membranes ; of the 
stroma, in abscesses and fibrous induration ; of the follicles, in their 
dilatation with purulent serum. If the inflammation of the ovary is 
the primary lesion it is usually confined to one organ. The stroma 
of the ovary is infiltrated with serum and pus, and may contain ab- 
scesses of large size. In other cases the ovary itself is but little 
changed, but is surrounded by a mass of fibrinous and purulent exu- 
dation. Such idiopathic forms of inflammation may terminate in 
recovery ; or the abscesses may perforate into the rectum and va- 
gina ; or the ovary is left indurated and bound down by adhesions ; 
or the patient dies from the violence of the disease. 

Acute inflammation of the ovaries unconnected with the puerperal 
condition is not common, but it may occur in connection with acute 
or chronic peritonitis or perimetritis. It is usually confined to one 
ovary. Either the follicles, stroma, or capsule, or all together, may 
be involved. The inflamed follicles are enlarged, their walls thick- 
ened ; they may contain bloody or purulent fluid. The stroma be- 
comes infiltrated with serum or pus, and later we may find abscesses 
or fibrous induration of the organ. The inflammation of the capsule 
may lead to the formation of membranous adhesions between the 
ovary. Fallopian tube, and surrounding parts. 

Chronic Intet'st It lal Oophoritis is not infrequently preceded by 
an acute inflammation, or it may gradually develop as an indepen- 
dent condition, often determined by some mechanical interference 
with the blood current. The ori;-au mav be increased in size, ov.'inu* 



602 



THE ORGANS OF GENERATION. 



to the formation of loose cellular or of dense, firm, new connective 
tissue. Under tliese conditions the blood vessels, especially the 
veins, may be Avidely dilated, and cysts in varying niunber and size 
may be present (Fig. 27Q). Sometimes the new-formed dense con- 
nective tissue may be largely limited to the surface of the organ, so 
that the albuginea may become so dense and thick that the f im.ctions 
of the organ must, as it would seem, be permanently interfered with. 
T7nder these conditions the surface of the ovary may be smooth or 
rough. 

On the other hand, the organ may be smaller than normal as the 
result of the formation of dense new interstitial connective tissue, and 
its surface greatly roughened and distorted. Sometimes the f orma- 




FiG. 276.— Chronic Oophohitis with dilated Blood Vessels a>-d Cysts. 

a, dense connective-tissue stroma; b, dilated veins; c. cysts; d. cyst with granular contents; 
e, cortical zone of immature Graafian follicles. 



tion of new dense tissue mav be lara^elv confijaed to the walls of the 
arteries, which become prominent and tortuous. Obhterating en- 
darteritis is not infrequently present. The atrophied ovary may be 
largely made up of thick- walled arteries and fibrous masses which 
are the result of incomplete resolution of the corpora lutea (Fig. 






Sometimes a more or less extensive hyperplasia of cells in the 
corpus luteum leads to the development of larger or smaller new- 
formed, convoluted, nodular masses in the ovarv, which are sometimes 
regarded as tumors. These structures may, according to Freeborn, 
soften at the centre and thus give rise to a special form of small 



THE ORGANS OF GENERATION. 



603 



ovarian cyst. Certain sarcomata of the ovary appear to originate 
in such an hyperplasia (see Fig. 278). 

Tubercular Inflammation of the ovaries is rare, and may ac- 
company tubercular inflammation of other organs, particularly the 
peritoneum and Fallopian tubes. It usually results in the production 
of cheesy nodules of considerable size. 

Syphilitic Inflammation in the form of gummata is uncommon. 

TUMORS. 

Fibromata. — These tumors are not very common nor usually of 
great importance. They may be very small or of great size. They 
are usually dense in texture, and in a considerable number of cases 
seem to originate in the tissue formed in the closure of the ruptured 





i?5^»!iis^# 







Fig. 277.— Chronic Oophoritis with Atrophy. 
From a case of valvular disease of the heart with chronic metritis and endometritis, o, thick- 
ened and dense interstitial tissue; &, old corpora lutea; c, arteries with greatly thickened walls; 
d, dilated veins. 

Graafian follicle. They may contain cysts or be accompanied by 
cysts of the surrounding stroma. Papillary fibromata of the surface 
of the ovary are sometimes seen, and the growth may be transplanted 
from this situation to the general peritoneal surfaces (Fig. -2:9). 

Leiomyomata containing more or less fibrous tissue are of occa- 
sional occurrence. 

Sarcoma of the ovaries is not common. It is usually primary, 
but may be metastatic. It is usually of the spindle-collod variety, 
but may contain areas of spheroidal-celled tissue or more or loss 
fibrous tissue. The tumors may be hard or soft, and are apt to in- 
volve both ovaries. 

Chondroma of the ovaries is described, but is rare ; cartilage not 
infrequently occurs, however, in dermoid cysts. 



604: 



THE ORGANS OF GEXERATIOX. 



Carcinoma^ usually of the glandular variety, may occur as a 
primary tumor of the ovary. It may be due to a continuous infec- 
tion from neighboring organs, or more rarely it is of metastatic ori- 
gin. Although the glandular medullary carcinomata are the most 
common, scirrhous, melanotic, and colloid cancer sometimes occur. 
Some forms of carcinoma stand in very close relation with certain of 
the cystic adenomata (see belovr). 

Adenomata (Cystic Adenomata ; Compound Ovarian Cysts). — 
These growths, which may occur in one or both ovaries, form one of 
the most common and iiiaportant classes of ovarian tumors. Some 
of their most noteworthy and important features depend ui)on their 




Fig. 278. — ComrEKCEHENT of S>4eco5£atoi:^ Growth in the Ovaby. 
From hyperplastic cells of corpus luteum. Specimen prepared by Dr. G. C. Freeborn. 

tendencv to the formation of cvsts. It should be remembered, how- 
ever, that the piimary lesion is a ti'ue new formation of glandular 
tissue, and not, as in the case of most cysts, a transformation, by re- 
tention or other^vise, of pre-existing structures. 

The growth primarily consists of a fibrous stroma, in which are 
tubular f oUicles lined with cylindrical epithehum. Or, in some cases, 
it consists of papiUary outgrowths from a fibrous stroma, which are 
covered with cylindrical epithelium. 

Glandular Cyst- Adenoma. — There is, as above stated, a marked 
tendency, particularly in the glandular form of adenoma, to a dilata- 



THE OKGANS OF GENERATION. 



005 



tion of the follicles by a semi-fluid material, and the formation of 
cysts. There may be a number of follicles equally dilated, so as to 
form a number of cysts of moderate size ; or only a few follicles are 
enormously dilated to form a large multilocutar cyst with but few 
compartments. The walls of the cysts may fuse together and be ab- 
sorbed, so as to form one large cyst divided by incomplete septa — uni- 
locular cysts. The stroma in which the follicfes and cysts are em- 
bedded may be largely developed or very scanty. 




Fig. 279.— Papilloma op Peritoneum. 
Transplanted from a similar growth on the surface of the ovary. 

The walls of the larger cysts are composed of fibrous tissue which 
is dense in the outer layers, more cellular in the inner, upon which 
the ej)itheliinn is placed. They may be thin and membranous, or we 
find devoh^ped on their internal surfaces an intracystic growth ooni- 
posod of a fibrous stroma and tubular follicles. These secondary 
follicles may also be filled with fluid and form larger and smaller 
cysts. The intra,cystic growths may be so large as to fill up the 
original cysts. Sometimes the intracystic groAvth presents very little 
dilatation ot' its follicles, so that the entire tumor has more the cha- 
racter of a solid growth than of a, (\vst. 
5-i 



606 



THE ORGANS OF GEXEKATIOX. 



Tile cylindrical epitlielium lining the cysts usually forros a single 
layer (Fig. 2S0), but, owing to the accumulatioii of fluid, the cells 
may become flattened and atrophied; or they may be fatty or desqua- 
mated. The contents of the cvsts differ considerablv in different 
cases, and even in different cysts in the same case. They may ]>e 
tough and ropy, or gelatinous or serous : transparent and colorless, 
or yellow or reddish, or reddish-brown : or they may be turbid and 
colorless, or variously colored — red, brown, or chocolate. 

Chemically the cyst contents, ^svhen thick and ropy, contain mucin 
or paralbumin, and perhaps other less ^vveU-known compounds belong- 
ing to the same class. It is believed that the peculiar r : t :y cl r iter 
which the fluid often possesses is due to the paralbumin, but the 
chemical nature and relations of this substance are still matters of 











-."rV .%- 



Tr -- .. - . -. ^'wV ■.'^•', ./^ 




Fig. 2K' —Crsnc Adzkoiu. of Ovabs. 
Giaadnlar f<xnn . 



dispute. It is probable that the contents of these cysts are, so far 
as the mucin and paralbumin are concerned, produced by a meta- 
ni : 2 ii jsis of the protoplasm of the lining cells, similar to that by 
which the mucin is produced in the mucous glands and in mucous 
membranes. We frequently find the cylindrical cells presenting the 
form CI :he s_-::."-led *• beaker cells. *' a_l in ^ __:r :; — - the mucous 
contents of the cysts are seen to be c:::.! .s with the -:m:h r con- 
tents of the beaker cells. It is probable that much of the fluid con- 
tents of the cysts c ::r.-- :: : __. -::nple trail- hi:" i_, 

Alicroscopically the e-: i-T-n: - : f these cy-:- v i ; - t1_~ -l -' :■ : n -: :Ierable 
variation. TVe mav find ahn :st no struct luaj. e^Tin-rnis ; or there 
may be red blood cells in v?:: " hr quantity, and pus cells in various 
staees of erannlar or fatrr It ^rn. ration or of disintesrration. s<d that 



THE ORGANS OF GENERATIOX, 



607 



variously shaped fragments of the cells appear. Then we may find 
cylindrical, or flattened, or polyhedral cells, either well preserved, 
swollen, or in a state of fatty degeneration (Fig. 281), or we may 
find fragments of these cells. It is these various forms of cells, often 
more or less swollen and in a condition of more or less well-marked 




Fia. asi.— Cells from Contents of an Ovarian Cyst in a Condition of Fatty Degeneration. 

granular and fatty degeneration, which have been considered cha- 
racteristic of the ovarian cysts and are sometimes called Drysdales 
corpuscles. While, however, they are of frequent occurrence under 
these conditions, they are by no means pathognomonic, since we find 
them in the contents of various kinds of cysts and cavities where the 
>cells are undergoing degeneration. In addition to the above struc- 




Fig. 282.— Cystic Adenoma op Ovary (Papillary form). 

tural elements we may find free fat droplets, cholosterin crystals, 
pigment granules, and more or less granular detritus. The material 
filling these cysts is sometimes called colloid, and the cysts are fre- 
quently called colloid cysts ; but we believe that the above view of 
their nature is the correct one. 

N'umerous secondary changes are liable to occur in these cysts. 



608 



THE ORGAXS OF GENERATION. 



The cells may become fatty and peel off, so that we may find in some 
parts only a connective-tissue wall. The walls may atrophy, may 
become infiltrated with salts of hme, or contain concentrically lamel- 
lated hme concretions. Inflammatory changes may occur in them. 
There may be a suppurative inflammation of the walls leading to 
the formation of abscesses, or pus may be mingled with the cyst 
contents ; the epithelium may be exfoliated and granulation tissue 
may form in the walls. Chronic inflammation may lead to consider- 
able thickening of the walls and to adhesions with neighboring parts. 
Haemorrhages, sometimes very extensive, may occur in inflammation, 
or as the result of other disturbances of the circulation, so that some 
of the cysts may be filled with blood. Inflammatory softening, gan- 
grene, etc., of the walls may lead to perforation, so that the contents 




VJ 0*^:^ lUi*^- -«^^ 





Fig. 283.— Multiple PAPn4LARY Cysts of the Omesttm, secoitdary to a similar Geo^wth in the 

Ovary. 

The papillary outgrowths are themselves becoming softened at their centres, forming acces- 
sory cysts. Drawn from specimen loaned by Dr. G. C Freeborn. 

of the cysts may be discharged into the peritoneal ca^dty, or, in 
virtue of adhesions, into the bladder, vagina, or rectum. Carcinoma 
may be developed from the epithelium of the cysts. Since these 
cysts sometimes reach a very large size, they may produce the greatest 
variety of disturbances in the abdominal cavity, which need not be 
enumerated here. 

They probably originate in the glandular epithelium of the ovary 
either before or after the formation of the Graafian f olhcles. ^ 



^For more extended descriptions of the cyst- adenomata of the ovaries see Wal- 
deyer, "Die epithelialen Eierstocksgesch^iilste," Archiv fiir Gvnakologie, Bd. i., 
Heft 2, pp. 252-316, 1870. Also Klebs, " Handbuch der pathologischen Anatomie," 
vierte Liefening, p. 796, 1873. Pozzi, "Treatise on Gynaecology," edited by Brooks 



H. Wells, M.D., 1892. 



THE ORGANS OP GENERATION. 



G09 



Papillary Cyst- Adenoma. — This form of cyst-adenoma was 
formierly regarded as but a variety of the form above described — a 
variety characterized by papillary outgrowths in caulifiower-like 
tufts from the walls of the cysts, which often in large degree fill the 
cyst spaces (Fig. 282). There appears, however, to be sufficient evi- 
dence, both anatomical and clinical, to justify the separation of the 
papillary from the glandular form of cyst-adenoma. 

The papillary cyst-adenomata are not, as a rule, as large as the 
glandular form. The cysts are fewer and they do not contain colloid 
material. The papillary outgrowths often break through the cyst 




mwmxmmMn 

















FlO 284.— AdENO SARCOIVfA OF THE OvARY. 

Specimen loaned by Dr. G. C. Freeborn. 



walls, and may be transplanted to the peritoneal or other surfaces in 
the form of multiple cystic or papillary tumors (Fig. 283). The 
papillae and cyst walls may be lined by cylindrical and often by cil- 
iated epitheHum. They may develop from the follicular or germinal 
epithelium, and probably, according to Williams, sometimes from 
the tubular epithelium. ' 

Cyst-adenomata of the ovary may, through an unusual prolifera- 



* Williams, "Contributions to the Histogenesis of the Papillary Cystoniata of the 
Ovary." Gives literature. BuHetiu of the Johns Hopkins Hospital, vol. ii., No. IS, 
December, 1891. 



610 THE ORGANS OF GENERATION. 

tion of the epithelial cells, form such dense, closely packed cellular 
masses that the type of structure seems changed. Such a change is 
shown in Fig. 284, in which, in addition to the excessive production 
of epithelium, the stroma is sarcomatous. 

Follicular Cysts of the Ovary. — The Graafian follicles may be 
dilated so as to form cysts. This may occur in one or both ovaries, 
and the cysts may be small or large, single or multiple. They are 
usually found after middle life, but may occur during youth, child- 
hood, or even in the foetus. The follicles dilate from the accumula- 
tion of fluid within them ; the ovum is destroyed, the epithelium 
flattened. The contents are usually serous and colorless, but may be 
viscid, turbid, purulent, or variously colored, red, yellow, or brown. 
The ovary may be crowded with numerous cysts of moderate size, 
whose adjacent walls may coalesce and atrophy, forming communi- 
cations between them. 

A variety of this form of cyst is formed by the dilatation, either 
with or without the hyperplasia above described, of a corpus luteum. 
Such cysts may communicate with a Fallopian tube. 

Dermoid Cysts. — These cysts may be uni- or multilocular, are 
usually of moderate size, but sometimes become as large as a man^s 
head or larger. Their fibrous walls may be thick or thin, and por- 
tions of the internal surface may present more or less completely de- 
veloped cuticular structures, such as corium, papillce, epidermis, hairs 
and hair follicles, sebaceous glands, etc. The cavity may contain a 
thick, whitish, greasy material composed of fiattened epithelium, fat, 
or cholesterin crystals. Or the cavity or walls may contain massed 
of irregularly formed hair, teeth, bone, cartilage, striated muscle, 
and nerve fibres and cells. Such growths, which are doubtless of 
embryonal origin, may exist for many years without causing incon- 
venience ; but inflammatory changes may occur in them, leading to 
adhesions and perforations into adjacent organs. They may form 
the nidus for the development of carcinoma, or they may calcify. 

In addition to the above-described adenoid, dermoid, and simple 
follicular cysts, there are a number of composite forms of not infre- 
quent occurrence. Thus, in connection with dermoid cysts or sepa- 
rately, we find larger and smaller cysts lined with ciliated epithe- 
lium. Then there are several cases described of cysts which partake 
of the characters of both adenoid and dermoid cysts. Such cysts 
may be multilocular and be lined with flattened, cylindrical, or 
ciliated epithelium, and may contain epidermal cells, cholesterin or 
mucin, etc. 

Small cysts, sometimes pediculated, sometimes not, of doubtful 
origin and usually of no special significance, are frequently found 
growing from the broad ligament near the ovary. The walls are^ 



THE ORGANS OP GENERATION. 



611 



usually very thin, lined with flattened epithelial cells, and the con- 
tents serous. 

Cysts of the Parovarium ^ lying between the peritoneal layers of 
the broad ligament, are usually small, but may be as large as a man's 
head. They are usually lined with ciliated epithelium, but some- 
times with flattened non-ciliated cells. The contents may be serous, 
or may be thick and contain mucin and paralbumin. 

THE FALLOPIAN TUBES. 
MALFORMATIONS. 

Absence of both tubes occurs with absence of the uterus. One 
tube may be absent, with arrested development of the corresponding 




Fig. 285.— Hydro salpinx. 

side of the uterus. Both tubes may be imperfectly developed ; either 
of their ends may be closed ; they may be inserted into the uterus at 
an abnormal place ; they may terminate in two or three abdominal 
ostia. 

CHANGES IN POSITION AND SIZE. 

The Fallopian tubes may participate in the various malpositions 
of the uterus and ovaries ; but they are most frequently displaced by 
the contraction of adhesions formed in perimetritic and periovarial 
inflammations. 

The lumen of the tube may be partially or completely closed as 
the result of inflammation of the mucous membrane : of peritonitis 
about the fimbriated extremity ; of tumors or inflammation of the 



612 THE ORGANS OF GENERATION. 

uterus ; or by pressure from without, or by adhesions, tumors, etc. 
It may become stopped by plugs of mucus or pus. 

Dilatation of the tubes may be produced by an accumulation of 
catarrhal or other exudation, when there is partial or complete ste- 
nosis at some portion of the tube. The dilatation may be moderate, 
converting the tube into a tortuous, sacculated canal containing 
mucous or serous fluid ; or, more rarely, large cysts may form con- 
taining several pounds of serous fluid — hydrosalpinx (Fig. 285). 
As the fluid collects the epithelium may become flattened or fatty 
or may desquamate. As a result of an inflammation in the walls of 
the dilated tube, the contents may be mixed with pus or blood. Rup- 
ture of a dilated tube sometimes occurs ; or severe and even fatal 
haemorrhage may take place into its cavity. Papillary growths 
are sometimes found springing from the inner wall of the cysts. 

HEMORRHAGE. 

Hsemorrhage into the tube may occur in puerperal women with 
retroversion of the uterus, with abortions ; hgematometra and tubal 
pregnancy ; in acute infectious diseases. The blood may undergo 
degenerative changes and be largely absorbed, or it may escape into 
the peritoneal cavity and cause peritonitis. 

INFLAMMATION (SALPINGITIS). 

Catarrhal Inflammation of the mucous membrane of the Fallo- 
pian tubes commonly occurs in connection with endometritis, fre- 
quently in the puerperal condition. In the acute stage the mucous 
membrane is hypersemic and swollen, and covered with a muco- 
purulent exudation. The inflammation may subside, leaving no 
lesions, but it more frequently becomes chronic, and may then result 
in peritoneal adhesions, thickening of the walls, obliteration of the 
tubes, dilatation, etc. 

Suppurative Salpingitis, — This inflammation of the mucous 
membrane may assume a suppurative character, particularly in con- 
nection with puerperal metritis and peritonitis, but sometiraes as a 
result of gonorrhoeal inflammation. 

Under these conditions the wall of the tube may be involved and 
pus may exude from the abdominal ends. It is difiicult, in many 
cases of suppurative salpingitis associated with peritonitis, to say 
which is the primary lesion. 

In some cases there is a considerable collection of pus in the tubes, 
causing dilatation— p^o-saZpma:. These collections may rupture 
into the peritoneal cavity, or the pus may escape into a cavity shut 
in by adhesions, or may perforate into the intestine or bladder. Or 
it may dry and finally become calcified. 



THE ORGANS OP GENERATION. 013 

Suppurative salpingitis is believed to be most commonly caused 
by the gonococcus or the pyogenic bacteria. 

Tubercular Inflammation. — This form of inflammation in the 
tubes is most frequently seen in its later stages, when the mucous 
membrane is partially or entirely converted into a thick, cheesy, 
often ulcerating layer. The lumen of the tubes may be dilated, the 
walls thickened from chronic inflammation. This lesion may occur 
by itself, or may be associated with tubercular inflammation of the 
lungs, or of the other genito-urinary organs, or of the peritoneum. 
The lesion usually commences at the abdominal ends of the tubes, 
;and both tubes are apt to be involved. 

Syphilitic Inflammation, in the form of a diffuse thickening of 
the wall by gummatous tissue, has been described. 

TUMORS. 

Small fibromata and fibro-myomata sometimes occur in the 
wall of the tubes or in the fimbriae. Small lipomata have been seen 
between the folds of the broad ligament in close connection Avith the 
tubes. 

Carcinoma of the tubes is usually, if not always, secondary to 
.carcinoma of the uterus or the ovaries. 

Cysts, usually of small size, sometimes pediculated and ^yiih. thin 
walls, are frequently seen in the peritoneal covering of the tubes or 
in the fimbriae. They are believed to be of embryonal origin. 

Dilatation of the tubes, as above described, may convert them 
into cyst-like structures. 

EXTRA-UTERINE PREGNANCY. 

Tubal Pregnancy. — The impregnated ovum is in some way hin- 
dered from passing into the uterus, becomes fixed in the tube, and 
is there developed. The villi of the chorion grow into the mucous 
membrane of the tube, forming an incomplete placenta. Rare cases 
are recorded in which the placenta was situated in the uterus while 
the foetus was developed in the tube. The embryo and its mem- 
branes are developed until they reach such a size that the tube sur- 
rounding them ruptures. This may occur in the first month or not 
until much later. In rare cases, when the wall of the tube was ex- 
tensively involved in the formation of the placenta, the development 
has gone on until term. The ovum maj^ remain in the tube after the 
rupture ; or may escape into the peritoneal ca^-ity, still enveloped in 
its membranes ; or the membranes may be ruptured and left in the 
tube. The rupture is generally attended wiih fatal ha-^morrhage. In 
some cases death is caused by the rupture of a dilated vein while the 



614 THE ORGANS OF GENERATION. 

tube is still intact. Hsemorrhage into the sac may occur before its. 
rupture. 

In rare cases death does not take place and the foetus is shut in 
by adhesions and false membranes. The embryo soon dies. In fa- 
vorable cases there is a slow absorption of the soft parts of the foe- 
tus, the bones are separated and left embedded in a mass of fibrous 
tissue, fat, cholesterin, and pigment ; or the foetus retains its shape 
and becomes mummified, and may then be encrusted with the salts 
of lime. 

In unfavorable cases degeneration and gangrene of the foetus take 
place rapidly, ^vith inflammation and suppuration of the surround- 
ing tissues. There may be perforation and escape of the broken- 
down foetus through the rectum, vagina, bladder, or abdominal wall. 
The patient may die from peritonitis or exhaustion, or may recover 
after the escape of the foetus. 

In some cases the foetus may escape through a rupture of the tube 
into the space between the folds of the broad ligament. 

Tubo- abdominal Pregnancy is produced by the development of 
the ovum in the fimbriated extremity of the Fallopian tube. Adhe- 
sions are formed, so that the foetus is partly in the end of the tube and 
partly in the abdomen. 

Interstitial Pregnancy. — The ovum in these cases is arrested 
and developed in the portion of the tube which passes through the 
wall of the uterus. 

Abdominal Pregnancy. — The ovum, after escaping from the 
ovary, does not enter the Fallopian tube, but becomes fixed to the 
peritoneum, usually at some part near the ovary. It is surrounded 
by thickened peritoneum and develops in that position. 

Ovarian Pregnancy. — The existence of this form of pregnancy is 
doubtful and difiicult to prove, but there are some cases in which it 
seems probable that the ovum develops in its Graafian follicle. The 
placenta may be attached to the tube or to the abdominal wall. 

In all forms of extra-uterine pregnancy the uterus becomes en- 
larged and a sort of decidua is formed on its internal surface. 

LESIONS OF THE PLACENTA. 

Aside from the variations from the normal in size, shape, and po- 
sition, for a description of wliich we refer to the works on obstet- 
rics, we may briefly mention here sorae of the more important struc- 
tural changes which the placenta may undergo. 

Hcemorrhage. — This may occur either on the maternal surf ace in_ 
the decidua ; or between the foetal surface and the membranes ; or irt 
the substance of the placenta. The latter form of hsemorrhage con- 



THE ORGANS OF GENERATION. 015- 

stitutes the true placental apoplexy. This may occur as the result 
of rupture of a placental sinus. The placental tissue is crowded 
apart, and a blood clot, often infiltrating the parenchyma, is formed. 
This may lead to abortion, or the blood may undergo disintegration 
and absorption and its place be occupied by a cicatrix. The placen- 
tal tissue in its vicinity may undergo fatty degeneration. Under 
other conditions, without evidence of rupture of the vessels, the pla- 
cental tissue may become infiltrated with blood in the form of an in- 
farction. In this, degenerative changes similar to the above may oc- 
cur, leading to fibrous induration of the placenta. 

The so-called '^ white infarctions '' of the placenta appear to be al- 
tered thrombi in the maternal blood spaces. They consist of lamel- 
lated or homogeneous or fibrillar fibrin, and form important larger 
and smaller yellowish-white or reddish, irregular masses, and appear 
to be of pathological significance only when they occur early or are 
of great extent. 

INFLAMMATION (PLACENTITIS). 

Suppurative Inflammation of the placenta, with the formation 
of abscesses, is of rare occurrence as the result of injury. 

Chronic Indurative Inflammation of the placenta may result 
in the formation of circumscribed masses of cellular and loose, or 
dense and cicatricial, connective tissue, or in a diffuse formation of 
connective tissue, which may interfere with the nutrition of the f oetu& 
and cause abortion. The new-formed connective tissue may undergo 
fatty degeneration or calcification. 

In another class of cases the new connective tissue is formed 
mainly in the walls of the vessels, particularly the arteries. This 
may occur in circumscribed portions of the vessels, leading to nodular 
growths around the arteries, or it may occur extensively along the 
various ramifications of the vessels, converting them into thick 
fibrous cords. The change is primarily in the adventitia, but all the 
coats of the vessel may become involved, leading to more or less 
complete obliteration of the lumen. 

Various proliferative and indurative changes in the placenta may 
occur as the result of syphilitic infection. 

DEGENERATIONS. 

Fatty and amyloid degeneration and calcification of the placental 
tissue are of not infrequent occurrence. 

Cysts of the placenta are of occasional occurrence ; their origin is 
in most cases obscure. ' 



1 See Ahlfeldt, Arch, fur Gynilkoloiile, Bil. ii., p. 307. Fcnomenodes, ibid.. 15d, 
XV., p. 343. llofmcicr, '' Die moiischliche Placenta," 1890. 



■616 THE ORGANS OF GENERATION. 

Fragments of placenta remaining in the uterus after delivery may 
serve as a nidus for a blood thrombus, or they may undergo prolifer- 
ation, thus compromising the uterine structures. 

An hypertrophy of the villi of the chorion may give rise to the 
fibrous structures known as fibrous moles. When to the fibrous 
change mucous degeneration is added the so-called hydatid moles 
.are formed. 

THE MAMMA. 
MALFORMATIONS. 

Absence of both mammse is only found in connection with other 
:marked malformations. 

Absence of one mamma has been observed in a few cases, with 
and without defective development of the corresponding half of the 
i;horax. 

Absence of one or of both nipples is more common. 

Arrest of development of the mammae is found in connection with 
arrest of development of the organs of generation, and, to a less 
degree, alone. 

Supernumerary mammae and nipples have been observed in a 
number of cases. The glands may all secrete milk during lactation. 

Too early development of the mammae is sometimes found in 
young children in connection with abnormal development of the 
organs of generation. 

HEMORRHAGE. 

In young women who suffer from amenorrhoea or dysmenorrhoea, 
small haemorrhages sometimes occur in the mammae at the time of 
menstruation. The blood may find its way into the milk ducts and 
exude in small quantities at the nipple. 

Contusions of the breast may produce extravasations of blood in 
the mammary gland or the surrounding connective tissue. This may 
become absorbed, or may remain and be surrounded by fibrous tissue 
or be converted into cysts. 

INFLAMMATION. 

During lactation the nipple is liable to become inflamed in three 
ways, which may occur separately or be combined together. 

1. The epidermis is rubbed off by nursing, the cutis becomes in- 
flamed and converted into granulation tissue ; in t.his way small or 
large ulcers may be formed. 

2. Fissures are formed at the base of the nipple, which extend 
completely through the skin, and are lined at the bottom with granu- 
lation tissue. 



THE ORGANS OF GENERATION. 



017' 



3. There is a diffuse inflammation of the whole nipple, which does, 
not, however, go on to suppuration. The nipple is conical, red, 
swollen, and very painful. 

There is a form of eczema-like inflammation of the nipple and 
areola which tends to ulcerate and develop into carcinoma. This is 
known as Paget's disease, and is believed by some observers to be 
associated with coccidia (see page 104). 

Acute Inflammation of the Mamma (Mastitis) occurs most fre- 
quently during lactation ; it also occurs during pregnancy, and 
occasionally in women who are neither pregnant nor nursing. 







Fig. 286.— Suppurative Mastitis occurring in the Non-functionatixg Gland. 

a, milk duct; 6, interstitial tissue; c, dense collections of pus; d, diffuse infiltration of lobule 
with pus. 

The inflammation may involve the subcutaneous connective tissue, 
the gland itself, or the connective tissue between the gland and the 
wall of the thorax. The inflamed tissues are at first congested, 
swollen, hard, and painful. The inflammation may stop at this point 
and resolution take place, but more frequently it is succeeded by 
suppuration. If the inflammation invoh'os the subcutaneous con- 
nective tissue the abscess mav be superficial and soon open througli 
the skin. If the gland is involved one lobule after another may 



:618 



THE ORGANS OF GENERATION. 



^become inflamed (Fig. 286), so that successive abscesses are formed 
in different parts of the gland. If the connective tissue beneath the 
gland is inflamed a deep abscess of large size may be formed, which 
usually perforates through the skin, but sometimes into the pleural 
cavity. In both these latter forms of abscess there is apt to be ne- 
crosis of large portions of tissue. These abscesses may cicatrize, or 
they may pass into a chronic condition and remain as suppurating, 
fistulous tracts for a long time. Suppurative mastitis is usually due 
to the presence of Streptococcus and Staphylococcus pyogenes. 

In new-born children there is often a painful swelling of the 
breasts, which usually subsides in a few days, but may go on to 
suppuration. 

Epidemic parotitis is sometimes complicated by mastitis. 

Chronic Inflammation of the interstitial connective tissue of the 




Fig. 287.— Chronic Inflammation of Mammary Gland. 



mammary gland may result in the formation of dense connective 
tissue (Fig. 287), with or without cystic dilatation of the milk ducts 
and atrophy of the glandular elements. Acute exudative inflamma- 
tion may occur in a gland which is the seat of chronic inflammation, 
and abscesses may be formed. 

Eczema sometimes affects the skin of the nipple. Attention has 
lately been drawn to the relationship between this inflammation and 
carcinoma of the nipple, for the two are frequently associated. It is 
possible that the eczema may lead to the subsequent development of 
the carcinoma. 

Tubercular Inflammation of the mammary gland and its excre- 
•tory ducts is of occasional occurrence. It may manifest itself in the 
form of mihary tubercles, larger and smaller cheesy masses of new- 
formed tissue, or cold abscesses. 



THE ORGANS OF GENERATION. 



G19 



Syphilitic ulcers may occur in the nipple either as primary chan- 
cres or as mucous patches. Gummy tumors have been observed in 
the mamma. 



TUMORS. 



There may be a general hypertrophy of one or both breasts. 
This is usually found in young, unmarried women, but sometimes in 







^^tz^^^:-^^^ 



^^^^^^"^^/^^i^^CI^Ja. 



Fig. 288.— I^fTRACANAIiIc^T^AB Fibroma of the Mamma, x 170 and reduced. 
Cross-section of a milk duct with polypoid ingrowths. 

advanced life. There is an increase in all the elements of the gland, 
both the glandular and the connective-tissue. 

Cysts of the mamma seem to be for the most part retention cysts, 
formed by the dilatation of the glandular ducts or acini. During 
lactation such retention cysts are sometimes formed, and then con- 
tain milk. They may reach an enormous size. At other times re- 
tention cysts are formed containing serous or viscid, brownish lluid^ 



620 



THE ORGANS OF GENERATION. 



which often exudes through the nipple. These cysts may be large or 
small, single or multiple. There is usually at the same time some 
growth and induration of the connective tissue of the gland. In 
some cases there are polypoid outgrowths of connective tissue from 
the wall of the cyst. These cysts are not to be confounded with the 
cysts which are developed "with the intracanalicular tumors, of which 
we shall speak below. 

Fibroma. — Circumscribed tumors composed of connective tissue 
are sometimes found in the breast. They are dense and hard, and 
may enclose in them some of the gland ducts and acini. 

Intracanalicular Fibroma. — These tumors are formed by a dif- 













fM 



'['f^ 



m^ 



r.- 



^. 



U- 



:1 ^^^;iJ£^m- ^V: 



*'y>'h^/H^' 



t< 




^/: 






5^ 



-N^~^ "^i-'^ 




Fig. 289.— Pericajjaliculab Fibroma of the Mamma. 



fuse growth of connective tissue, a dilatation of the milk ducts, and 
a growth of polypoid fibrous tumors from the walls of the ducts into 
their cavities. The glandular acini may be atrophied, or enlarged, 
or cystic. A section of such a tumor looks like a solid mass of fibrous 
tissue, divided by clefts and fissures lined with cylindrical or cuboidal 
epithehum (Fig. 288), or containing cysts into which project poly- 
poid fibrous outgrowths. These tumors grow slowly, but if left to 
themselves may reach an enormous size. The skin over them may 
ulcerate and the tumor project through the opening in fungous 
masses. 

Pericanalicular Fibroma. — Sometimes the new connective tissue 
forms a more or less thick cylindrical investment of the duct with- 



THE ORGANS OF GENERATION. 621 

out growing into its lumen. This formation, which is shown in Fig. 
289, is sometimes called pericanalicular fibroma. 

Myxoma, — This form of tumor may occur as a circumscribed 
growth replacing part of the mamma, or it may be developed in the 
same way as the intracanalicular fibromata. It is not uncommon in 
these intracanalicular tumors to find a combination of fibrous, mu- 
cous, and sarcomatous tissue in the same tumor. 

Chondroma is a very rare form of tumor in the mamma. A few 
cases have been described in which it was combined with carcinoma. 

Adenoma. — Tumors composed of glandular acini, and ducts sur- 
rounded by connective tissue, are of frequent occurrence in the mam- 
ma (Fig. 128, page 2G3). They are either single or multiple, or sev- 
eral may be developed successively in the same breast. They grow 
at first slowly, afterward more rapidly. Their structure may be 
further complicated by the dilatation of one or more of the ducts 
which compose the tumor into cysts, and the ingrowth of connective 
tissue from the walls of these cysts. 

Sarcoma. — This form of growth may be developed as a circum- 
scribed tumor of small or large size. Its basement substance is that 
of connective or of mucous tissue, and may be scanty or abundant. 
The cells are spheroidal, fusiform, branched, or polygonal. These 
tumors may simply replace the gland ; or glandular acini and ducts 
may be enclosed within them ; or these ducts and acini may be di- 
lated so as to form cysts ; or there may be a new growth of the gland 
tissue so as to form an adeno-sarcoma. 

In other cases the sarcoma takes the intracanalicular form. 
There is a diffuse growth of sarcomatous tissue, a dilatation of milk 
ducts, and an outgrowth of sarcomatous tissue from the walls of the 
dilated ducts into their cavities. These tumors often reach an enor- 
mous size, and there is apt to be ulceration of the skin over them. 

Carcinoma of the mamma is most common in w^omen between 
the ages of thirty-five and fifty-five, but it sometimes occurs in 
women not over twenty years old, and sometimes in old persons. It 
occurs in either breast, in the right rather more frequently than in 
the left, but sometimes in both. The growth begins more f requently 
at the periphery of the gland than at its centre, and more frequently 
in the upper edge of the gland than in any other place. 

The growth most frequently begins as a small, circumscribed 
nodule, which enlarges and involves more and mcn*e of the breast : 
sometimes, however, it is diffuse from the first, and sometimes it be- 
gins in the nij^ple. 

It may infiltrate the adjacent tissues and the axillary and cer^'ical 
glands, and form metastatic tumors in different parts of the body. 
There are several different anatomical forms of the growth : 
55 



« 



622 THE ORGANS OF GEXERATIOX. 

1. Those ill which the epithehal elements preponderate, the soft 
or so-called medullary carcinomaia. 

2. Those in which both the connective-tissue stroma and the 
epithelial cells are prominently developed, the cells lying in well- 
defined larger and smaller irregular-shaped spaces, so that the simu- 
lation of gland tissue is tolerably close. These are called carcinoma 
simplex. 

3. The tumors in which the connective-tissue stroma preponder- 
ates, giving the tumor its hard, dense character. This is the carci- 
noma fibrosum, or scirrhous. 

Colloid carcinoma of the mamma is rare. Various secondary 
changes may occur in these tumors, such as have been described in 
the section on Tumors. 

In any of these forms of cancer there may be cystic dilatations of 
the ducts and acini. 

Besides the primary carcinomata of the mamma, secondary car- 
cinomata are met with in rare cases. 



MALE GEXERATIVE 0IIGA:N'S. 

THE PEXIS. 

MALFORMATIONS. 

Entire absence of the penis is met with in connection ^^dth great 
defects of development of the rest of the body. 

Absence of the penis, with proper development of the other 
organs of generation, is rare. The urethra then usually opens into 
the rectum. 

An abnormally small penis is found, with absence or arrested de- 
velopment of the testicles. 

Absence or a rudhnentary form of the prepuce has been observed 
in a number of cases. Congenital phimosis is also not infrequent. 

Hypospadia consists in an arrest of development of the penis 
and scrotum. In its highest degree the penis is one-half to one inch 
long, the glans penis small and resembling a clitoris. On the lower 
side of the penis is a deep cleft lined with mucous membrane. Into 
this cleft the urethra opens at the root of the penis. The scrotum 
remains separated into two halves, resembling labia majora. The 
testes descend into their proper position on each side or remain in 
the abdomen. If the testicles continue to develop normally the in- 
dividual has the appearance and capacities of a man ; if their de- 
velopment is arrested the indi^ddual is small and has a womanish ap- 
pearance. 



THE ORGANS OF GENERATION. 62 



Q 



In lesser grades of the same malformation the two halves of the 
scrotum are joined and the penis is larger, but a part of the urethra 
remains open as a cleft at any point of the penis. 

Epispadias is an opening of the urethra on the upper side of the 
penis. It presents various grades and forms. 

Hermaphroditism. — This is a union of two sexes in the same 
person, the test of which is the presence of the secreting organs, the 
ovaries and testicles. True hermaphroditism is rare, but it does 
occur, while most of the conditions called hermaphroditism are in 
reality due to varying malformations of the external generative 
organs. 

Pseudo-hermaphroditism. — This malformation consists in an 
abnormal change in the transition from the foetal condition of the 
parts to their fully developed form. In the male, normally, the 
greater part of Miiller's canal disappears and its lower end forms the 
vesicula prostatica. In this malformation Miiller's canal is changed, 
as it is in the female, into Fallopian tubes, uterus, and vagina, w^hile 
at the same time the testes, epididymes, vesiculse seminales, and 
spermatic cord are formed as usual. In the lesser degrees of this 
malformation we find, in the place of the vesicula prostatica, a pear- 
shaped sac as large as a pigeon's e^g, with muscular walls and an 
epithelial lining. This sac may be incompletely divided into a ute- 
rus and vagina, and it opens into the urethra. In the higher grades 
we find a well-formed vagina and uterus. The uterus may or may 
not have Fallopian tubes. The testicles are usually retained in the 
abdomen or inguinal canals, and are small. The spermatic ducts 
run on the sides of the uterus and open into the urethra or are 
closed. The penis and scrotum appear as in hypospadia, or are well 
formed. The appearance of the individual varies with the develop- 
ment of the testicles. 

True Hermaphroditism may be lateral. In this condition there 
is hypospadia ; a vagina and uterus and a Fallopian tube and ovary 
on one side, and a testicle and spermatic cord on the other. 

In certain cases, which may be called bilateral hermajjhrodit- 
ism, there is a testicle on one side and an ovary on the other.' 

Enlargement of the penis is sometimes caused by venous conges- 
tion from heart disease ; by long-continued .masturbation, as a result 
of which the corpus cavernosum may lose its contractility : and in 
rare cases by hypertrophy of the stroma of the corpus cavernosum. 



' For a detailed consideration of the malformations of the male and female gene- 
rative organs consult Klebs, " Ilandbuch der pathologisehen Anatomie." and more re- 
cent cases of hermaphroditism by i/£'^)j97ie7', Arch, f . Anat. u. Physiol., ISTO, and by 
Hofmann, Wien, med. Jahrb., 1877. 



634 THE ORGANS OF GENERATION. 

Injury and Hcemorrliage. — Injuries to the penis are liable to 
give rise to severe hsemorrhage on account of its peculiar vascu- 
lar character ; suppurative inflammation, gangrene, infiltration with 
urine and its consequences, are also liable to occur. The contractions 
of the cicatricial tissue by which wounds are healed frequently give 
rise to various distortions of the organ and not infrequently prevent 
subsequent erections. 

INFLAMMATION. 

Balanitis, inflammation of the prepuce, is usually produced by 
gonorrhoea or by accumulations of smegma. The skin is red and 
swollen and may ulcerate. Condylomata may be formed, and adhe- 
sions between the prepuce and glans. The glans may ulcerate and 
the prepuce may be much thickened. If the prepuce is long there is 
an inflammatory phimosis, and the products of inflammation accu- 
mulate within the swollen prepuce. In some cases the prepuce be^ 
comes gangrenous. 

Paraphimosis is produced by the retraction of a narrow prepuce 
behind the glans, with consequent stricture, inflammation, and some- 
times gangrene. 

Inflammation of the Corpora Cavernosa may be the result of 
injury, may follow fistulse, may occur in connection with inflamma- 
tion of the connective tissue of the pelvis, and may accompany the 
acute infectious diseases, such as pysemia, small-pox, measles, ty- 
phus, etc. It may result in fibrous induration of portions of the cor- 
pora cavernosa ; in rare cases in abscesses or diffuse purulent infil- 
tration ; sometimes in gangrene. Tubercular inflammation of the 
penis has repeatedly followed circumcision performed by uncleanly 
tubercular persons. 

Syphilitic Ulcers frequently occur on the glans penis and pre- 
puce. The indurated chancre is formed either from an excoriation 
in which a pustule is formed or from a little nodule. The pustule 
breaks and its walls are infiltrated with small round cells. The 
nodule softens, breaks down, and forms an ulcer, of which the walls 
are infiltrated with cells in the same way. 

Syphilitic condylomata are of frequent occurrence on the glans. 

Phagedenic ulcers occur and may destroy a considerable part of 
the penis. Herpes of the prepuce occurs in the form of small vesicles^ 
which may later become ulcers. Erysipelatous and furuncular in- 
flammation sometimes involves the skin of the penis. 

TUMORS. 

Papilloma is found on the prepuce and glans penis. It occurs in 
the form of little warty growths, or of composite, cauliflower masses. 



THE ORGANS OF GENERATION. 625 

even as large as a fist. In either case the structure is the same — '■ 
hypertrophied papillae covered with epithelium. Sometimes the epi- 
thelial layers become thick and horny, forming large, dense projec- 
tions. 

Fibroma diffusum, or elephantiasis of the prepuce, may occur, 
leading to immense thickening of the structure. It consists in a dif- 
fuse growth of the deep fibrous tissue of the cutis. Lipomata, 
angiomata, circumscrihed fibromata, and sebaceous cysts may 
occur in the penis. Carcinoma of the penis usually occurs in the 
form of epitheliomata. These are most frequent in the prepuce and 
glans penis. They may have the form of flat ulcers, or of infiltrat- 
ing, ulcerating nodules, or very frequently assume the form of 
papillary outgrowths, which may attain great size, ulcerate, or un- 
dergo a variety of infiammatory changes. These growths may in- 
volve the entire skin of the penis ; they may invade deeper parts. 
The inguinal glands may be invaded. Distant metastases may occur, 
but are not frequent. 

Glandular carcinoma of the penis is not common. It may be sec- 
ondary to carcinoma in some other part of the body. 

Calcification and Ossification of the connective tissue of the 
corpora cavernosa sometimes occur. Large and small prei^utial cal- 
culi are occasionally found between the prepuce and the glans. 
These may be formed in situ, may come from the bladder or from 
without, and may later increase in size. 

THE SCROTUM. 

The skin of the scrotum is subject to the various forms of lesions 
which may occur in any part of the integument. 

Elephantiasis of the scrotum consists in the main of a develop- 
ment of new connective tissue from the cutis, which is sometimes ac- 
companied by dilatation of the lymph vessels. The thickened scrotum 
sometimes forms very large tumors, often rough upon the surface, 
which may entirely cover in the penis. Lipomata, fibromata, 
atheromatous or sebaceous cysts, and dermoid cijsts containing 
hair, bone, cartilage, etc., are sometimes found. Occasionally the 
skin of the scrotum is beset with numerous lar<;'er and smaller seba- 
ceous cysts, which raise the surface into little globular or wart- like 
projections. Epitheliomata, in the form of flat or papillary ulcerat- 
ing tumors, are of frequent occurrence among chinmey sweepers, 
and may lead to extensive ulcerations of the adjacent parts and in- 
volvement of neighboring lymph nodes. 

Dermoids and Teratomata of the scrotum are not uncommon. 
In very rare cases tumors containing a. ccnisiderable portion of a 
foetal skeleton have been found in the scrotum. 



Q26 THE ORGANS OF GENERATION. 

THE TESTICLES. 
MALFORMATIONS. 

Absence of both testicles, either with or without absence of the 
epididymes, spermatic cords, and vesiculse seminales, occurs in rare 
cases. The scrotum is only indicated or may contain the epididymes. 
The penis is small, and the individuals are small and poorly de- 
veloped. 

Instead of being entirely wanting, the testes may be imperfectly 
developed. The individuals are weakly and effeminate. Absence 
of one testicle, with healthy development of the other, is more fre- 
quent. The corresponding epididymis and cord may be absent or 
present. 

The spermatic cords and vesiculse seminales may be absent or im- 
perfectly developed on one or both sides, while the testes are normal. 

Either one or both testicles may remain permanently in their 
foetal position, or may not descend into the scrotum for several years 
after birth (cryptorchismus). Their descent may even be delayed 
until the thirtieth year of life. This condition may depend on an 
arrest of development in the testes or the gubernaculum testis ; on 
adhesions produced by intra-uterine peritonitis ; on narrowing of the 
inguinal canal ; on narrowing or shortening of the vaginal process 
of the peritoneum ; or on abnormal size or position of the testicle. 
Usually the malformation is confined to one testicle, and then is more 
frequent on the left side. The testicle is usually found in the abdo- 
men close to the mouth of the inguinal canal, or in the inguinal 
canal just below the external ring ; but it may be beneath the skin 
in the perineum, or in the crural canal with the femoral vessels, or 
elsewhere. The retained testis is usually not fully developed, or 
undergoes fatty or fibrous degeneration. The retention of one or 
even of both testicles does not preclude the possibility of procreation. 
Retained testicles are prone to inflammatory changes and liable to 
become the seat of malignant tumors. 

Sometimes, while the testis is retained, the epididymis and sper- 
matic cord descend into the scrotum. In rare cases the position of 
the testis may be changed so that the epididymis and cord are in 
front. The existence of a supernumerary testis has been asserted in 
some cases, but is rather loubtf ul. 

Atrophy of the testicle may occur in old age or in persons who 
are in a condition of premature senility ; or as the result of pressure 
from herniaB, hydrocele, or inflammatory products. 

HYDROCELE. 
Hydrocele of the tunica vaginalis consists in an accumulation of 



THE ORGANS OF GENERATION. 027 

serum in the cavity of this membrane. It is usually confined to one 
side. It is caused by acute or chronic inflammation of the tunica 
vaginalis, by varicocele, or by general dropsy. The serum is found 
in small or in large quantities ; it is usually transparent, may contain 
cholesterin, or be purulent and contain the pyogenic bacteria, or be 
mixed with blood. The tunica vaginalis remains unchanged, or is 
thickened, or contains plates of bone, or is covered with polypoid 
fibrous bodies which fall off and are found free in the cavity of the 
sac. There may be adhesions between the layers of the tunica vagi- 
nalis, and in this way the fluid becomes sacculated. The testis is 
pushed downward and backward ; it remains unchanged or is atro- 
phied. 

Hydrocele of the processus vaginalis consists in an accumulation 
of serum in the cavity of the vaginal process of the peritoneum, 
which remains open after the descent of the testicle. There are sev- 
eral different varieties. 

(a) The vaginal process is entirely open and there is a free com- 
munication with the peritoneal cavity. The serum may originate in 
the cavity of the peritoneum or of the vaginal process, and passes 
freely from one to the other. 

(b) The processus vaginalis is closed in the inguinal canal, while 
its lower portion is filled with serum. 

(c) The processus vaginalis is closed about the testis and the vis- 
ceral layer of the tunica vaginalis is formed. The serum accumu- 
lates in the upper part of the vaginal process which communicates 
with the peritoneal cavity. 

(d) The vaginal process is closed in the inguinal canal and over 
the testis ; the serum accumulates so as to form one or more sacs 
between these two points. Inguinal hernia may complicate this form 
of hydrocele. 

Hydrocele of the spermatic cord consists in a general a?dema of 
the connective tissue of the cord, or in the development of circum- 
scribed cysts in this connective tissue. 

A peculiar form of hydrocele is produced by the accumulation of 
serum in the sac of an inguinal hernia, from which the intestine has 
become retracted. 

SPERMATOCELE. 

Cysts containing spermatic fluid not infrequently arise from the 
epididj^mis or from the rete testis. These sometimes acquire a 
large size and crowd the tunica vaginalis before them, so that they 
simulate a collection of fluid in the cavity of the latter. The wall of 
the cyst may be lined with ciliated or with flattened epithelium. 
The contents are sometimes simply serous, but more fretiuently opal- 
escent and contain great numbers of spermatozoa. 



628 THE ORGANS OF GENERATION. 

HEMATOCELE. 

Hsematocele of the tunica vaginalis consists in an effusion of 
blood into the cavity of this sac. It may be produced by injury ; in 
scurvy, or the hsemorrhagic diathesis ; or it may complicate a pre- 
existing hydrocele. The effused blood usually soon degenerates, 
and we find the sac filled with a brownish fluid or a thick, grumous 
mass. The tunica vaginalis may be thickened. The testis remains 
normal or is atrophied. 

Effusion of blood into the loose connective tissue of the scrotum 
is often called extravaginal hcematocele. 

Hsematocele of the spermatic cord occurs in rare cases as a dif- 
fused infiltration of blood in the connective tissue of the cord. Or 
blood may be effused into a hydrocele of the cord. 

INFLAMMATION. 

Inflammation of the testicles may be caused by injuries, exposure 
to cold, inflammation of the urethra, syphilis ; or it may occur in 
parotitis and in connection with various infectious diseases. The 
testes, epididymis, or tunica albuginea may be principally involved. 
Usually only one testicle is inflamed, sometimes both. The inflam- 
mation may extend to the vas deferens. The inflammation may be 
acute or chronic. 

Acute Orchitis is most frequent in the epididymis and tunica 
albuginea. When the testis is involved the organ is congested and 
infiltrated with serum or pus. From this condition it may return to 
the normal state ; or small abscesses may form which may be ab- 
sorbed, or they may increase in size so as to involve nearly the entire 
organ. They may perforate externally, and then healing may occur 
by means of granulation tissue ; or extensive gangrenous destruc- 
tion of the scrotum may occur. They may become enclosed in a 
fibrous capsule, and the contents dry and become cheesy or calcified, 
and so persist for a long time. The acute inflammation may pass 
over into the chronic form. Acute epididymitis is frequently the 
result of gonorrhoeal infection, and may or may not be associated 
with inflammation of the testis. 

The products of inflammation may collect in varying quantity in 
the lumina of the seminiferous tubules and in the ducts of the epidi- 
dymis, and the epithelium of these structures may degenerate. 

Chronic Orchitis occurs as a sequel of acute inflammation or as 
an original condition. It may affect the testis, the epididymis, or 
the spermatic cord. The seminiferous tubules may be filled with des- 
quamated and degenerated epithelium ; they may be atrophied, or 
their walls may be greatly thickened so that they are converted into 



THE ORGANS OF GENERATION. 



029 



dense fibrous cords, with almost or quite complete obliteration of their 
lumina. There is usually a marked increase in the interstitial tissue, 
which causes atrophy of the tubules (Fig. 200). The albuginea may be 
greatly thickened. In some cases the testis is converted into a mass 
of dense connective tissue, in which but little trace of the original 
structure can be made out. The new-formed coi.nective tissue may 
become calcified. A periorchitis may lead to thickening and union 
of the layers of the tunica vaginalis testis. Abscesses are not infre- 
quent in connection with chronic orchitis. 

Tubercular Orchitis may occur in connection with tuberculosis 

a 







Fig. 290.— Chronic Interstitial Orchitis with Atrophy of the Seminiferous TrBULES. 

a, thickened interstitial tissue; c, thickened merabrana propria of the tubules; d, separated 
-epithelial cell mass in the lumen of the tubules. 

of the other genito-urinary organs or the lungs, in acute general 
miliary tuberculosis, or by itself. It usually begins in the epididy- 
mis and may extend from there to the testis, or it may commence in 
the testis itself. The appearances which the testicles present, when 
the seat of this form of inflammation, are exceedingly varied and 
difficult of interpretation. This is partly due to the complex struc- 
ture of the organ, partly to the varied complicating simple inflam- 
matory changes which the difl:erent parts of the organ undergo in 
-connection with the special tuberciflar inflammation, and the impos- 



630 THE ORGANS OF GENERATION. 

sibility of making any definite morphological distinction between: 
them. Further researches are urgently needed in this direction, and 
it seems probable that in the presence or absence of the tubercle 
bacillus we shall find the needed differentiating factor between va- 
rious inflammatory processes which are at present grouped under the 
general heading of tuberculosis testis. 

We may find in the testicle small circumscribed masses of cells, 
visible to the naked eye as whitish spots, which are sometimes com- 
posed of small spheroidal cells or of larger polyhedral or fusiform 
or round cells. These occur in the walls of seminiferous tubules and 
blood vessels, and in the interstitial tissue. Sometimes associated 
with these smaller nodules, and sometimes not, we find larger, ir- 
regular yellowish or gray cheesy masses, which are believed by many 
to be formed by the confluence and degeneration of the smaller 




Fig. 291.— Chronic Orchitis with the Formation op Structures resembling Miliary Tubercles.. 
a, thickened interstitial tissue ; b, mass of granular cells in the interstitial tissue; c, thickened 
membrana propria of seminiferous tubule; d, mass of separated epithelium in tubule; e, accumula- 
tion of small spheroidal cells around tubules; /, thickened membrana propria enclosing g, a multi- 
imclear mass resembling a giant cell. 

nodules. The cheesy masses may break down and open externally, 
giving rise to fistulse, gangrenous inflammation, etc. Hand-in-hand 
with this nodular formation of tissue, which is disposed to degenera- 
tive changes, there are various more or less diffuse alterations of the 
parenchyma and interstitial tissue of the organ which must not be 
overlooked, and which often constitute a most prominent and im- 
portant factor in the lesion. The interstitial tissue may be more or 
less densely and diffusely infiltrated with small spheroidal cells. The 
arteries are often the seat of obliterating endarteritis. The walls of 
the seminiferous tubules may be very much thickened, so that the 
lumen may be entirely obliterated. The epithelium lining the tubules 
may be fatty, disintegrated, and peeled off, or it may have largely 



THE ORGANS OF GENERATION. 631 

disappeared. The lumen of the tubules may he filled with a granular, 
nucleated mass which in transverse sections hjoks like a giant cell. 
The thickened walls of the tubules may be infiltrated with small 
spheroidal cells, so that the underlying stroma is scarcely visible. 
When this occurs in connection with a similar infiltration of the in- 
terstitial tissue and the formation of giant cells in the lumina, we 
have structures which present the greatest resemblance to some 
forms of tubercle granula (Fig. 291). 

Tubercular inflammation may extend from the testis to the vas 
deferens, vesiculse seminales, and prostate. 

Syphilitic Orchitis. — This may occur in the form of a diffuse 
new formation of connective tissue, which may occur in some par- 
ticular part of the organ or be widely distributed through it, and by 
reason of which the organ becomes dense and firm. Morphologically 
there is no difference between this form of orchitis and chronic in- 
durative orchitis from other causes. It may occur in children affected 
with congenital syphilis. Gummata may form in connection with 
the interstitial induration. These may disappear, leaving irregular 
cicatrices. 

Inflammatory foci in the testicle are common in leprosy. 

TUMORS. 

Fibroma occurs in the form of small dendritic or polypoid growths 
of the visceral layer of the tunica vaginalis. These sometimes be- 
come free and are found in the sac, usually in connection vnth hydro- 
cele. Small nodular fibromata occasionally occur in the albuginea 
and in the spermatic cord. 

Lipomata, either pure or in combination with myxoma and sar- 
coma, may arise from the connective tissue of the spermatic cord or 
from the tunica albuginea. 

Chondroma, sometimes in a pure form, but more frequently com- 
bined with myxoma and sarcoma, occurs in the testicles and may 
attain a large size. Osteoma has been described. 

Sarcomata occur in the testes and epididymis, most frequently 
in the former. They present the greatest variety in structure. They 
may be composed of spheroidal or spindle-shaped cells ; they may be 
soft or contain much fibrous tissue ; they are very frequently com- 
bined with myxoma, chondroma, lipoma, etc. Owing to the occlu- 
sion of the seminiferous tubules, cysts may be formed in these sarco- 
mata. In these cysts polypoid growths of sarcomatous tissue may 
occur in the form of intracanalicular growths. Thus the so-called 
cysto-sarcomata of the testicle are formed. The walls of those cysts 
may coalesce, so that large, irregular cavities may be formed. AVheu 
the cysts are not filled by polypoid outgrowths from their walls they 



632 THE ORGANS OF GEXERATIOX. 

may contain a mucous, serous, or bloody fluid, cr masses of flattened 
cells, fat, and cliolesterin. The CYsts mav be lined with cylindrical, 
ciliated, or flattened cells. 

Rhahdomijomata have been several times observed, frequently in 
combination with cysts. 

Adenoma is occasionally found, usually in combination wdth sar- 
coma or carcinoma, or with cyst formation. 

Carcinoma of the testicle is commonly of the soft medullary 
form, of rapid growth, and usually primary. It may commence in 
the testis or epididymis. Usually only one testicle is involved. Fre- 
quently the entire glandular portion of the organs is replaced by the 
new growth. The albuginea expands with the growth of the tumor, 
and may continue to enclose it even when of large size. The tissues 
are often very vascular, and hsemorrhages, areas of softening, fatty 
and mucous degeneration are frequent. The inguinal and lumbar 
lymph nodes are apt to become involved, and distant metastasis may 
occur. Karely the growth assumes a scirrhous form. 

Cysts. — Aside from the above-mentioned cysts which occur in 
connection with tumors and si^ermatocele, cysts may be formed from 
persistent remnants of Mliller's canal in the epididymis, or from ob- 
struction of the seminiferous tubules or ducts by inflammatory pro- 
ducts or tissue. 

Dermoid Cysts of various kinds are of infrequent occurrence, and 
are sometimes quite complex in character. They may be embedded 
in the substance of the gland. Probably some of the above-men- 
tioned cystic rhabdomyomata belong here. 

PARASITES. 

Ecliinococcus may occur in the testis or epididymis. 

THE SEMINAL VESICLES. 

The seminal vesicles may be the seat of acute or chronic inflam- 
mation, which is most frequently connected with inflammatory 
changes in adjacent parts, prostate, urethra, etc. As a result of 
chronic inflammation the vesicles may be atrophied, or they may be 
greatly dilated as a result of constriction of the ducts. 

Tubercular inflammation is usually secondary. Carcinoma of the 
rectum or other genito-urinary organs may secondarily involve the 
seminal vesicles. Small concretions, sometimes containing masses of 
permatozoa, are occasionally found in the seminal vesicles, 

THE PEOSTATE. 

Hypertrophy of the prostate is a frequent senile change ; it is 
general or partial. • 



THE ORGANS OF GENERATION. 633 

In general hypertrophy the entire organ is enlarged and may 
reach the size of a man's fist. The enlargement is symmetrical, or is 
most marked in one half or in the so-called middle lobe. The organ 
is hard and dense, or soft or alveolar, containing numerous small 
openings from which a turbid fluid exudes. These different appear- 
ances depend upon the character of the hypertrophy. The muscular 
and fibrous tissue alone may be increased, which is most common, or 
at the same time the glandular tissue, or the glandular tissue alone. 
In the latter case the lesion is more properly an adenoma. The in- 
crease of muscular tissue properly constitutes a myoma. 

In partial hypertrophy we find circumscribed nodules of muscular 
tissue or of muscular and glandular tissue. They are usually situ- 
ated at the periphery of the organ and project into the bladder. 
They may become detached from the prostate, and are found as 
small, movable tumors beneath the mucous membrane of the blad- 
der. 

Both forms of hypertrophy frequently produce, by pressure, reten- 
tion of urine and changes in the bladder. 

Atrophy oi the prostate is sometimes seen in connection with 
atrophy of the testicles, with castration, and as a result of inflamma- 
tion. Sometimes the ducts of the glandular portion are enlarged, or 
there may be fibrous degeneration of the organ. 

INFLAMMATION. 

Inflammation of the prostate is caused by gonorrhoea, by injuries, 
or, more rarely, is idiopathic. It may run an acute or chronic course. 
The gland may after a time return to its normal condition, or is grad- 
ually converted into a mass of fibrous tissue filled with abscesses. 
The abscesses may perforate into the bladder, urethra, vesiculfe 
seminales, rectum, or peritoneum. Or the inflammation may extend 
to the connective tissue of the scrotum or beneath the pelvic perito- 
neum. The pus may become thickened and cheesy, or even calcified. 

Tubercular Inflammation of the prostate usually accompanies 
a similar lesion of some of the other genito-urinary organs, and 
is rarely of primary occurrence. Large cheesy masses are often 
formed, which may break down and open into the bladder or rec- 
tum. 

TUMORS. 

Adenoma of the prostate occurs in one of the forms of hypertro- 
phy of the gland, either with or without an increase in the fibro- 
muscular interstitial tissue. 

Carcinoma is of occasional occurrence, and may be primary or 
secondarv. 



634 THE ORGANS OF GENERATION. 

Cysts of the prostate are sometimes found either as a result of 
occlusion of the ducts by hypertrophy of the interstitial tissue, tu- 
mors, etc. , or as a result of faulty development. 

PARASITES. 

Echinococcus of the prostate has been described, but is rare. 

CONCRETIONS. 

Small ovoidal or spheroidal, often brown or black bodies, having 
the characters of corpora amylacea, are of very frequent occurrence 
in the alveoh of the prostate, particularly in old persons. We find 
a certain number of them in the prostate of nearly all old men, but 
they are sometimes present in great numbers. Larger, irregular 
concretions, apparently formed by the coalescence or growth of the 
smaller ones, are less frequently found, and may be encrusted with 
lime salts. These concretions may give rise to ulceration of the 
ducts of the gland or to interference with the passage of urine, but 
in a majority of cases they seem to be of little or no practical impor- 
tance. 

cowper's glands. 

These glands may be enlarged and encroach upon the lumen of 
the urethra, either in acute or chronic inflammation. Cysts formed 
by the closure of the excretory ducts may also project into the ure- 
thral canal. 

THE MALE MAMMA. 

There may be an abnormal number of mammae. In boys, at 
about the time of puberty, the mammae may be swollen and inflamed 
or they may secrete milk. Cases are recorded in which adult males 
possessed large mammae which secreted milk. The breasts may be 
enlarged from an increase of fat or of connective tissue. 

Cysts of the male breast are not very infrequent. Fibromata, 
sarcomata, cysto-sarcomata, myxomata, and various forms of car- 
ci?io?}za^a are recorded.^ 

^ For literature of tumor of male mamma see Gross, " Tumors of the Mammary 
Gland," p. 237. 



THE BOXES. 



DISTURBANCES OF CIRCULATION. 

Hypercemia. — The evidences of this condition are most marked 
to the naked eye in the periosteum and marrow, particularly the lat- 
ter. It should be remembered that the color of the marrow varies 
considerably under normal conditions, depending upon age and situ- 
ation. In the bones of the foetus and new-born, and near the areas 
of ossification in the young, the marrow is normally red in color. 
In adults the marrow of the sternum, vertebrae, and to a certain de- 
gree that of the ribs, pelvic and cranial bones, and the cancellous 
. tissue of the ends of the long bones, is red or reddish in color. But 
most of the marrow, particularly in long bones of the extremities, is 
of a yellowish color from the presence of fat cells. In old age the 
marrow of all the bones is apt to become pale, and to assume a more 
or less translucent or gelatinous appearance. 

Hypersemia usually occurs as an accompaniment of inflammatory 
processes in the bone, and, when marked, the periosteum is swollen 
and red'; the compact bone tissue may appear of a pink color, while 
the marrow, either by an increase in the amount of blood or absorp- 
tion of its fat, or both, may be of a uniform dark-red color or mot- 
tled with red and reddish-yellow. 

Hceniorrliage. — This may be due to wounds and injuries, to in- 
flammatory and necrotic processes ; and small haemorrhages often 
accompany scurvy, purpura, hnemorrhagic diathesis, and leukii?mia. 
Haemorrhages of considerable size between the periosteum and bone 
may lead to serious consequences, by cutting off the blood supply to 
the superficial layers of bone and thus inducing necrosis ; but when 
not in contact with the air they are not usually of serious import, since 
they are readily absorbed. The smaller luBmorrhages of the medulla 
are not usually of much importance. The decomposition of the ex- 
travasated blood may lead to extensive pigmentation of the marrow. 

WOUNDS, FRACTURES, AND DISLOCATIONS. 

For details of the varied alterations produced under these con- 
ditions, and the secondary changes involved in the healing process. 



636 THE BONES. 

we refer to the section on repair, page 98, and to works on surgery. 
It may be stated here, however, that the heahng of fractures occurs 
by the formation of granulation tissue in greater or less amount 
about the seat of fracture, and the direct formation of bone under 
the influence of osteoblasts, or by a preliminary formation of carti- 
lage or fibrous tissue and the gradual conversion of this into bone by 
metaplasia. 

INFLAMMATION. 

The periosteum, bone tissue, and marrow are so intimately con- 
nected that in most cases they all share to a greater or less degree in 
the pathological alterations of the bones. But as sometimes one, 
sometimes another is most markedly involved, it is convenient to 
consider separately here the inflammatory changes by which they 
are respectively affected. 

Periostitis. 

AYe may distinguish several varieties : 

1. Simple Acute Periostitis. — This form is apt to occur in chil- 
dren and ill-nourished persons from comparatively slight injuries or 
from unknown causes. The periosteum is thickened, succulent, 
congested, and more or less abundantly infiltrated with leucocytes, 
while the connective-tissue fibres are swollen. The periosteum be- 
comes less firmly adherent to the bone, and the cells of the inner 
layers are increased in number. This variety of inflammation may 
terminate in the disappearance of the new elements and complete 
resolution, or it may represent a preliixiinary stage of one of the 
other varieties of inflammation. 

2. Suppiuxttive Periostitis may begin as a simple or as a puru- 
lent inflammation. The pus is formed in the inner layers of the 
periosteum, and between it and the bone. The outer layers of the 
periosteum may resist for a long time the suppurative process. The 
accumulation of pus may dissect up the membrane from the bone 
and leave the latter bare. The pus thus formed may remain in this 
position for a long time, may be absorbed, may become dry and 
cheesy, or may burst through the periosteum and form abscesses in 
the soft parts. The bone, if separated froin its nutrient membrane, 
may remain unchanged, but more frequently necrosis or inflamma- 
tion of the bone itself is set up. Such a periostitis may run an acute 
or a chronic course. 

Sometimes suppurative peritostitis takes on a very malignant 
character. Pus is developed not only beneath but in the periosteum, 
forming abscesses filled with foul pus. The periosteum breaks down 
into a gangrenous, foul-smelling mass, and the same change may af- 
fect the neighboring soft parts. The medulla may take part in the 



THE BONES. 037 

process and break down into a purulent, gangrenous mass. Haemor- 
rhages may complicate the process. The lymphatic nodes are en- 
larged and swollen ; abscesses may form in different parts of the 
body, and the patient may die with the symptoms of pyaemia. The 
pyogenic cocci may be found, under these conditions, in the exuda- 
tions of the periosteum as well as in the metastatic abscesses. 

3. Fibrous Periostitis. — This is a slow, chronic form of inflam- 
mation, resulting in the formation of new connective tissue in the 
periosteum, which becomes thickened and dense and unusually adhe- 
rent to the bone. It may be the result of necrosis, chronic arthritis, 
chronic ulcers of adjacent soft parts, etc. It may follow a simple 
acute periostitis. 

4. Ossifying Periostitis results in the formation of new bone 
from the inner layers of the periosteum. The masses of new-formed 
bone, called osteophytes, are of variable shape. They may form a 
thin, velvet-like, villous layer ; or they are little spiculse ; or they 
form larger, rounded masses, or a thick, uniform layer extending 
over a large part of a bone. - They may be at first very loosely con- 
nected with the bone. The new bone has at first a loose, spongy 
character. It is formed of thin plates of bone enclosing large cavities 
filled with marrow. Layers of compact bone tissue are formed from 
the medulla on the sides of the original plates, and thus the medul- 
lary cavities are gradually filled up with bone. The new bone may 
thus become as compact or even denser than normal bone. The h3'per- 
ostoses and exostoses thus formed may remain indefinitely, or they 
may gradually become smaller and finally disappear by absorption. 

The formation of new bone in the form of osteophytes, or in dense 
masses beneath and in the periosteum, occurs as a result of the same 
process by which bone tissue is normally formed. Certain rather 
large cells, called osteoblasts, which are formed along the blood 
vessels, possess the power of depositing osseous basement substance 
about themselves and so forming bone. Pathological new forma- 
tion of bone differs from the normal mainly in the conditions under 
which it occurs. The blood vessels around which the pathological 
bone develops, which grow out of the old vessels, as in the formation 
of granulation tissue, are irregularly arranged and subject to a variety 
of abnormal nutritive and mechanical conditions, so that the new 
bone is not usuall}^ formed in a series of definite systems of lamellae, 
but, as above described, in a series of irregular spicul?e or masses. 
Moreover, as will be seen further on, the conditions under which it is 
formed being liable to change, and itself serving no definite purpose 
in the economy, as does normal bone, pathological new bone is often 
an evanescent structure. The details of its disappearance will be 
considered below. 
56 



638 THE BOXES. 

5. Syphilitic Periostitis. — Syphilitic poisoning may give rise to 
simple, purulent, fibrous, and ossifying periostitis. Or, in addition 
to these, gummy tumors may be developed in the periosteum. The 
bone tissue is usually more or less involved. The gummata may be 
absorbed or undergo cheesy degeneration, or be converted into fibrous 
tissue, or they may suppurate. 

6. Tubercular Periostitis. — In badly nourished persons, particu- 
larly in children suffering from so-called scrofula (see page 436), a 
chronic purulent periostitis is frequently associated with the forma- 
tion of miliary tubercles. Abscesses are apt to form in and about the 
periosteum, and Tvhen these are evacuated granulation tissue may 
develop, in which miliary tubercles are formed. In these tubercles 
the Bacillus tuberculosis may be found. The bone is apt to be in- 
volved to a greater or less extent in the form of inflammatory changes 

or caries. 

Osteitis. 

Inflammation in bone tissue is dependent upon the same general 
conditions and presents essentially the same series of phenomena as 
inflammation in other kinds of connective tissue. But it is variously 
modified in detail by the peculiar dense and unyielding character of 
the basement substance, and by certain peculiarities of the blood 
supply and the nutritive conditions under which the cells are placed. 
In simple exudative inflammation the same series of phenomena 
occur in connection with the blood A^essels, resulting in the production 
of serum, fibrin, and pus, as in other tissues ; but the extent to which 
these changes can occur is limited and constantly associated with 
striking alterations in the basement substance. It is these secondary 
alterations in the basement substance which lend to inflammations 
of the bone their most peculiar characters, and in the prominence 
which these assume the fundamental alterations are often overlooked. 
The most common of these secondary alterations are the absorption 
of the hard basement substance of the bone and its replacement by, 
or conversion into, young cellular forms of fibrillar connective tissue 
or marrow tissue, and the new formation, in more or less atypical 
manner, of new bone. As a result of these changes the bones in 
simple inflammation undergo alterations either in the direction of 
greater vascularity and increase of the spaces filled with granulation 
or marrow tissue, and so become more porous and less compact at the 
expense of the dense basement substance ; or they undergo alterations 
in the direction of an increase in density at the expense of new- 
formed or pre-existing marrow spaces. Or, as is frequently the case, 
both series of changes occur either simultaneously in different regions, 
or follow one another, or are variously associated together. Yery 
frequently one or the other of the opposing forms of alteration pre- 



THE BONES. 



639 



dominates, or one may occur to the exclusion of the other, and we 
thus have two prominent forms of inflammation, which are called 
rarefying osteitis or osteo-porosis, and condensing osteitis or 
osteosclerosis. The exact nature of the conditions under which in 
one case the bones become more, in another less dense, we do not 
understand. 

In addition to these phases of inflammation in bone, and in fre- 
quent and varied association with them, there are alterations leading 
to death and destruction of bone tissue in greater or less amount, 
which we call caries and necrosis ; and also inflammatory changes, 
more or less characteristic, due to the influence of peculiar specific 
agencies, such as the syphilitic and tuberculous infection, and we 




Fig, 292.— Rarefying Osteitis in Ulna of Child. 

a, isolated bone fragment with rough ed^es; b. marrow tissue; c, Howship's lacuna? with 
•osteoclasts. 



thus recognize tubercular and syphilitic osteitis. Again, the pro- 
duction of pus is so prominent a feature in some cases as to represent 
a purulent phase of the inflammatory process. Finally, any of these 
forms, and commonly several of them at once, are variously asso- 
ciated with more or less marked inflammatory or degenerative alter- 
ations of the periosteum on the one hand, or the marrow tissue on 
the other, or of both combined. 

Rarefying Osteitis consists essentially in the formation in the 
marrow spaces. Haversian canals, or beneath the periosteum, of 
new, very cellular and vascular tissue, resembling granulation or 
young marrow tissue, in connection with which, or under wlioso 
influence, the basement substance of the bone is absorbed. The 



640 THE BONES. 

absorption of the bone occurs chiefly in the same way in which 
the bone is absorbed in normal growth, namely, under the influ- 
ence of certain large cells, called osteoclasts, which are grouped 
around the blood vessels. If we examine a thin section of bone 
which is undergoing absorption (Fig. 292), we find the edges of the 
bone which border on the vascular surfaces irregularly indented by 
deep or shallow depressions, sometimes simple, sometimes quite com- 
plex. These are called Hoiv ship's lacunce and are usually filled or 
lined by larger and smaller granular, frequently multinuclear cells — 
the so-called osteoclasts. In the larger lacunae there may be granu- 
lation tissue with loops of blood vessels, with or without cells which 
have the morphological characters of osteoclasts. Under the influ- 
ence of these peculiar cells, or of the new vascular tissue, the bone 
is gradually absorbed. In other cases we find irregular branching 
channels through the bone across the lamellae, which appear to be 
due- to the enlargement and coalescence of the lacunge and canaliculi, 
without the direct influence of blood vessels or other cells than the 
fixed cells of the bone. The tissue which replaces the absorbed bone 
may be very rich in small spheroidal cells, or it may be more or less 
fibrillar. As a result of this process irregular islets of bone tissue 
may be entirely separated from adjacent bone and surrounded by a 
more or less fibrillar vascular tissue ; this is most apt to occur in the 
cancellous tissue. Or the originally compact bone may become 
traversed by a series of larger and smaller irregular branching, com- 
municating channels with ragged walls. These progressive altera- 
tions may cease and be succeeded by a new formation of bone along 
the edges of the channels or cavities ; it may result in necrotic 
changes ; the vascular changes may become prominent and suppura- 
tion ensue. 

Rarefjdng osteitis may occur as an idiopathic disease from un- 
known causes ; it is often associated with the scrofulous diathesis, 
with diseases of the joints, with fractures or other injuries to the 
bone ; it often forms a predorainant feature in tubercular inflamma- 
tion of the bones, etc. It is chiefly by a rarefying osteitis that bone 
tissue is eroded and destroyed in the vicinity of tumors, aneurisms, 
etc., which exert pressure on the bones. By the same process the 
sharp ends of fractured bones may be rounded off as heahng pro- 
ceeds. 

When this form of inflammation occurs in cancellous bone tissue 
the marrow is red or gelatinous, and the bony septa may disappear 
altogether, so that in extreme cases we may have, instead of can- 
cellous bone, a mass of granulation tissue. When the disease occurs 
in the articular extremity of a bone the granulating medulla may 
send little offshoots through the articular cartilage. These may 



THE BONES. 



641 



become fused together and inflammation of the joint follow. The 
walls of the shafts of the long bones may be converted into spongy 
tissue. If, as is sometimes the case, an ossifying periostitis occurs 
at the same time, the bone is thickened but spongy ; or sometimes 
there are concentric layers of compact bone tissue, separated by rare- 
fied bone. 

Condensing Osteitis (Osteo-sclerosis). — This lesion is character- 
ized by the new formation of bone in the walls of the marrow cavi- 
ties or Haversian canals. The bone is formed under the influence of 
the blood vessels and osteoblasts, as in normal bone formation, but 
ivith less regularity. It may result in the conversion of cancellous 
tissue into compact bone, in the filling-up of the medullary cavity of 







-^Tfi.?. 



Fig. 293 —Condensing Osteitis, or Osteo-sclerosis, op Ulna op Child. 

a, fragment of old bone with roughened, sinuous edges; 6, old Howship's lacunae covered with 
more recently formed bone lamellae. 

long bones with more or less dense bone tissue. The compact bone, 
owing to the filling of its Haversian canals, may become very dense 
and ivory-like. When the medullary cavities of long bones are in- 
volved the yellow marrow is converted into red marrow by the ab- 
sorption of fat and increased vascularity. It is frequently associated 
with ossif3ang periostitis. 

It very frequently follows rarefying osteitis, and under the micro- 
scope we can then often see the Howship's lacmuB resulting from the 
original absorption process filled and covered in with new bone 
lamella) (Fig. ^Oo). It is apt to occur in connection with necrosis or 
some chronic inflammation of adjacent soft parts, but it is sometimes 
idiopathic or occurs under unknown couditious. 



642 



THE BONES. 



Suppurative Osteitis (Abscess of Bone).— This process occurs 
usually in the ends of the long bones. It begins with a rarefying 
osteitis. The medulla undergoes actual suppuration, the bone tissue 
is destroyed, and a circumscribed cavity is formed in the bone, filled 
with pus and lined with granulation tissue. 

Less frequently abscesses are formed in the shaft of a long bone 
by a circumscribed suppuration of the medulla. These abscesses usu- 
ally occur in old people. They last for many years, have little ten- 
dency to perforation, may gradually enlarge and be accompanied by 
an ossifying periostitis, so that the bone is expanded. Very rarely 
acute suppurative osteitis, with rapid formation of an abscess, and. 
perforation, has been observed. 




Fig. 294.— Tubercular Osteitis. 
A miliary tubercle formed in the cancellous tissue near the joint in tubercular arthritis. 



In some cases, instead of abscess, there may be a diffuse infiltra- 
tion with pus of the Haversian canals or the spaces formed by rare- 
fying osteitis (see Osteomyelitis, page 644). 

Tubercular Osteitis is essentially a rarefying osteitis associated 
with the formation of tubercle tissue and cheesy degeneration. The 
tubercles are sometimes small, scattered, and miliary in form (see 
Fig. 294); sometimes they unite to form larger and smaller masses. 
There may be extensive involvement of the medulla. There may be 
much simple granulation tissue or the formation of abscess associated 
with the process. Condensing osteitis and necrosis are not infre- 
quently present. Tubercular osteitis is often associated with tuber- 
cular inflammation of the joints. It is most apt to occur in cancellous. 



THE BONES. 643 

bone tissue, and is most common in the bodies of the vertebrse and 
in the carpal and tarsal bone. Tubercle bacilli may be found in the 
tubercular masses, sometimes in considerable numbers. 

Syphilitic Osteitis. — The syphilitic poison may induce one of 
the above-mentioned varieties of osteitis, or it may produce gummy 
tumors. The gummatous osteitis usually commences in the peri- 
osteum, which becomes thickened and infiltrated with cells, so that 
there may be a circumscribed thickening of the periosteum, with 
or without distinct gummata. The vessels which extend from the 
periosteum into the bone become surrounded by new cellular tissue, 
which causes an enlargement of the canals. At this stage, if we 
strip off the periosteum, we drag with it the vessels surrounded by 
the new cell growth, leaving the bones beneath with numerous small 
perforations extending inward. As the disease progresses the gum- 
matous tissue around the vessels continues to increase, and the chan- 
nels in the bone enlarge by a rarefying osteitis and coalesce, form- 
ing large, irregular defects filled with gummatous tissue. In these 
masses of new tissue cheesy degeneration and the formation of 
fibrous tissue occur, giving them the characteristic appearance. In 
the vicinity of these gumma- filled spaces a condensing osteitis may 
occur, both in the substance of the bone and on the surface, in the 
form of osteophytes, so that the opening in the bone may be sur- 
rounded by an elevated, irregular ring of bone tissue. All this may 
occur beneath the uninvolved skin, or the skin may participate by a 
suppurative inflammation, resulting in ulceration. These processes 
may be circumscribed or involve a large part of a bone. It is not 
infrequently associated with necrosis of larger and smaller portions 
of bone. The gummatous tissue may be absorbed and its place be 
more or less filled with fibrous tissue. Syphilitic osteitis is most fre- 
quent in the cranial bones, but may occur elsewhere, as in the 
sternum, clavicle, tibia and fibula, the ribs, etc. 

Congenital Syphilis. — The bones of young children in this con- 
dition may occasionally show increased density or evidences of peri- 
ostitis, or irregular thickenings, particularly of the skull. The re- 
searches of Wegner,^ which have been frequently confirmed by 
other observers, have shown that exceedingly characteristic changes 
very uniformly occur in the long bones in still-born or young chil- 
dren who are the victims of hereditary syphilis. These changes are 
found for the most part along the border zone between the epiphysis 
and diaphysis. It will be remembered that, in normal ossification 
of the long bones, the border line between the calcification and ossi- 
fication zones is narrow, sharply defined, and straight, or gently and 



' Virchow's Arch., Bd. 1., 1S70. p. 805. 



644 THE BOXES. 

evenly curved. In the syphilitic bones, on the contrary, this line 
is broader, uneven, and presents various modifications, depending 
upon the stage of the disease. Wegner distinguishes three promi- 
nent stages, which, however, merge into one another, so that all in- 
termediate forms may be seen. In the first stage there may be seen, 
between the cartilage and the new-formed spongy bone, a white or 
reddish-white zone, about two mm. in breadth, with very irregular 
borders, consisting of calcified cartilage, in which the linear groups 
of cartilage cells are more abundant than normal. In the second 
stage the calcified zone, still containing an unusual number of carti- 
lage cells, is broader and still more irregular and less sharply out- 
lined against the ossification zone. The cartilage just beyond it is 
softer and almost gelatinous, and may contain numerous blood ves- 
sels, islets of connective tissue or of calcification, or irregular ossifi- 
cation. In the tliird stage the bone may be pouched out at the sides 
around the ossification and calcification zones, and the perichondrium 
and periosteum thickened. The whitish, irregular calcified zone is 
hard and friable. Between this and the new-formed bone there is an 
irregular, soft, gray or graj^sh-yellow zone, from two to four mm. in 
thickness, which forms a loose, readily separated connection between 
the cartilage and the diaphysis. The white, friable zone consists 
mainly of irregular rows of degenerated and distorted cartilage cells 
lying in a calcified basement substance, of irregular masses of atypi- 
cal bone tissue, and of blood vessels surrounded by variously shaped 
cells. The soft zone consists of more or less vascular tissue with 
homogeneous basement substance, and round and spindle-shaped 
cells. This soft zone is not sharply outlined against the adjoining 
new-formed spongy bone, which, instead of consisting of the nor- 
mal marrow spaces with bony lamellae between them, is largely com- 
posed of granulation tissue. 

Different stages of this faulty development may be seen in differ- 
ent bones in the same individual. According to Wegner the lesion 
is usually most advanced in the lower end of the femur, then in the 
lower ends of the leg bones and of the forearm, then in the upper 
ends of the tibia, femur, and fibula. 

'Not infrequently there is fatty degeneration of the marrow cells 
and blood vessels, giving the marrow a reddish-yellow color. These 
alterations of the bones may occur, not only in children who have 
gummata in other parts of the body, but also in those in which other 
evidences of syphilitic poisoning are absent. So uniform is their oc- 
currence that their presence alone suffices for the establishment of a 
diagnosis. 

OSTEOMYELITIS. 

In most of the inflammatory processes which affect the bones the 



THE BONES. Oio 

medulla has an important share, so that many conditions described 
as osteitis are really osteomyelitis. It is customary, however, to re- 
serve the latter name for those cases in .which the medulla is prima- 
rily or chiefly involved. Using the word in this sense, we may dis- 
tinguish a so-called idiopathic and a traumatic osteorayelitis. 

Idiopathic Osteomyelitis. — At the commencement of this dis- 
ease, which usually begins in the shaft of one of the long bones, there 
is hyperaemia and oedema of the medulla, so that if the bone be 
opened the marrow is soft and of a dark-red color. A diffuse sup- 
puration now rapidly ensues, and the marrow becomes streaked or 
mottled with gray. Occasionally, though not often, larger and 
smaller abscesses may form in the marrow. The inflammatory areas 
may be circumscribed and scattered ; or, in the more malignant cases, 
the entire marrow may become rapidly involved. The cancellous 
tissue of one or both of the epiphyses usually becomes involved. The 
disease, however, is not commonly confined to the medullary spaces. 
The periosteum becomes oedematous and infiltrated with pus, and 
the surrounding soft parts may become the seat of intense inflamma- 
tory changes. Abscesses of the periosteum or surrounding tissues 
are apt to form. As a result of these changes necrosis of greater or 
less portions of the bone may ensue. The medullary cavity may be- 
come enlarged as pus accumulates, and the wall of the bone may be 
broken through, permitting the discharge of pus outward. Some- 
times several bones may be involved at once. Secondar}" involve- 
ment of the joints is very frequent. There may be ovi\.j a serous or 
purulent exudation ; or the acute and destructive inflammatory pro- 
cess may extend to the joint and produce extensive alterations. In 
young persons the epiphyses very frequently become separated from 
the shaft by the destruction of the cartilage which binds them to- 
gether. 

In the severer cases, which are often denominated, par excellence^ 
malignant osteomyelitis, the changes may be very rapid and destruc- 
tive. The medulla becomes broken down and gangrenous ; the 
joints are soon involved ; large portions of the bone, sometimes the 
whole shaft, necrose ; the periosteum and surrounding parts become 
gangrenous ; the veins contain thrombi, and pyiiemic infarctions and 
abscesses may form in various parts of the body. 

These lesions are, in the large majority of cases at least, due to 
the presence and action of the pyogenic cocci, the Staphylococcus 
pyogenes and the Streptococcus pyogenes, and in many of its forms 
may be regarded as one of the phases of pviiemia. 

Traumatic Osteomyelitis. — This form of intlammatiou may bo 
the result of fracture, amputation, etc. It consists essentially in a 
more or loss diffuse suppurative intlammation of the marrow, vari- 



646 THE BONES. 

ously associated, depending upon the intensity and cause of the dis- 
ease, with necrosis, gangrene, periostitis, etc. In its more intense 
and destructive forms its lesions are similar to those of spontaneous 
osteomyelitis. Similar bacteria are found in the inflammatory foci, 
and metastatic pysemic abscesses may be formed in other parts of the 
body. 

The distinction, then, between the so-called spontaneous or idio- 
pathic infectious osteomyelitis and traumatic infectious osteomyelitis 
is a superficial one, dependent largely upon the general manner in 
which the pathogenic bacteria gain access to the body. ^ 

In the more chronic forms of osteomyelitis there is apt to be more 
or less ossifying periostitis and osteo-sclerosis, and fistulge may form 
in the bone, through which the exudations are discharged. 

NECROSIS. 

By necrosis we understand the death of a larger or smaller por- 
tion of bone. This condition is induced by causes which deprive 
the bone of its proper vascular supply from tho periosteum and 
medulla. Suppurative periostitis, osteomyelitis, and osteitis, trau- 
matic separation of the periosteum, ulcers of neighboring soft parts, 
emboli, the action of phosphorus vapor, and diseases, like typhus, 
which diminish the vitality, may cause necrosis. N'ecrosis is a pure 
form of gangrene, differing from gangrene of soft parts in that the 
dead bone has at first, and may retain for a long time, the general 
outward characters of normal bone ; while in dead soft parts the 
phenomena of decomposition, under the influence of bacteria, rapidly 
ensue, inducing marked complicating appearances in the dead tissue. 

When a portion of bone has died an inflammation is set up at 
the dividing line between the dead and li^ang bone. This inflam- 
mation has the characters of a rarefying osteitis (see above), and 
finally separates the dead from the living bone. The dead bone, or 
sequestrum, may remain smooth and unaltered, or it may be eroded 
by the influence of surrounding pus or granulation tissue or osteo- 
clasts. In this way it is possible for the sequestrum, if it be small, 
to be entirely absorbed. More frequently there is a production of 
new bone around the sequestrum, either beneath the periosteum or 
in the substance of the bone, and this becomes lined with granula- 
tion tissue, from which pus may continue to be formed, bathing the 
sequestrum. 

Necrosis may involve the superficial layers, or the entire thick- 

^ For bibliography consult Park, "Acute Infectious Processes in Bone," Am. 
Jour. Med. Sci., July, 1889. For the consideration of this condition in children see 
Koj^likand Van Arsdale, ibid., April and May, 1892. 



THE BONES. 647 

ness of the wall of a long bone, or only the spongy tissue and inner 
layers of the wall, or an entire bone, or a number of different por- 
tions of the same bone, but it is most apt to occur in compact bone. 

The death and separation of the bone are very soon followed by 
the growth of new bone to repair the loss. The periosteum, the 
medulla, and the surrounding soft tissues may all take part in this 
new growth. The new bone is usually irregular, rough, perforated 
with openings through which pus formed around the sequestrum 
may be discharged. If the sequestrum be removed healing may oc- 
cur by the formation of new bone ; but the bone is usually more or 
less distorted by the irregular new ossification. 

Phosphorus Necrosis. — Under the influence of phosphorus vapor, 
periostitis and osteitis, particularly of the jaw, are apt to occur, 
which usually lead to more or less extensive necrosis, usually associ- 
ated with prolonged and often extensive suppuration. 

CARIES. 

Caries of bone is essentially an ulcerative osteitis resulting in pro- 
gressive molecular destruction of the bone tissue. It differs from 
necrosis in that, in the latter, larger and smaller masses of bone die, 
while in caries the destruction is molecular and gradual. It may 
occur in connection with any form of osteitis, with periostitis and 
osteomyelitis, or it may be secondary to inflammatory or destructive 
processes in the joints or adjacent soft parts. The depressed surfaces- 
of bones in which caries is progressing are rough and more or less- 
finely jagged, and may be covered with granulations. The minute 
changes by which ulceration and destruction of the bone are produced 
in caries are somewhat analogous with those in rarefying osteitis, 
but there are marked degenerative changes in the bone cells, which 
may become fatty or converted into a granular material. Moreover, 
the basement substance of the bone, instead of being absorbed, may 
disintegrate, with the formation of larger and smaller masses of 
detritus. Sometimes the lime salts are removed from the basement 
substance, which is converted into atypical fibrillar tissue and fatty 
and granular detritus. Very extensive suppurations and necrosis 
may be associated with caries. 

Long-continued caries, especially in badly nourished individuals, 
is apt to become complicated Avitli tubercular inflammation. 

There is very little tendency to spontaneous healing in caries, but 
it may occur, and the defects produced may be more or less supplied 
by means of new-formed bone. 

RACHITIS (rickets). 

Rickets is a disease affecting the developniout of bone, prevent- 



€48 



THE BONES. 



ing its proper ossification. The disease iisually occurs during the 
first two years of life, but may be congenital, or may occur as late 
as the twelfth year. 

The physiological growth of bones depends upon three conditions. 
They grow in length by the production of bone in the cartilage be- 
tween the epiphysis and diaphysis ; in thickness, by the growth of 
bone from the inner layers of the periosteum. At the same time 
the medullar}^ canal is enlarged, in proportion to the growth of the 
bone, by the disappearance of the inner layers of bone. 

In rickets these three conditions are abnormally affected. The 
cartilaginous and subperiosteal cell growth, which precedes ossifi- 
-cation, goes on with increased rapidity and exuberance and in an 




)"e 



4 "^ 



-^ „ "^ i? » St 








Fig. 295.— Rachitic Bone. 
Showing ossification zone in a longitudinal section of a rib. 



irregular manner, both between the epiphyses and diaphyses and 
beneath the periosteum, while the actual ossification is imperfect, 
irregular, or wanting. At the same time the dilatation of the me- 
dullary cavity goes on irregularly and often to an excessive degree. 
If we examine microscopically the region between the epiphysis 
and diaphysis (Fig. 295), we find that the cartilage cells are not reg- 
Tilarly arranged in rows along a definite zone in advance of the line 
of ossification, as in normal development, but that there is an irreg- 
ular heaping-up of cartilage cells, sometimes in rows, sometimes not, 
over an ill-defined and irregular area. The zone of calcification also, 
instead of being narrow, regular, and sharply defined, is quite lack- 
ing in uniformity. Areas of calcification may be isolated in the re- 



THE BONES. 64^ 

gion of proliferating cartilage cells, or calcification may be altogether 
absent over considerable areas. 

Corresponding to these irregularities the ossification zone is also- 
irregular. New-formed bone and marrow cavities containing blood 
vessels may lie in the midst of the cartilage, or masses of cartilage 
may lie deep in the region which should be completely ossified. In 
other places it seems as if the cartilage tissue were directly con- 
verted into an ill-formed bone tissue by metaplasia or direct trans- 
formation. It will readily be seen from this that the medullary spa- 
ces of the new- formed bone are irregular, and this abnormality is 
enhanced by the premature intramedullary absorption of the bone. 

The same sort of irregularity in the bone formation may be seen 
beneath the periosteum. An excessive proliferation of cells in the 
inner layers of the periosteum, the irregular calcification which oc- 
curs about them, and the absence of uniformity in the elaboration of 
ill-structured bone, conspire to produce an irregular, spongy bone 
tissue instead of the compact, lamellated tissue which is so necessary 
here for the solidity of the structure. The increased cell growth be- 
tween the epiphyses and diaphyses produces the peculiar knobby 
swellings which are characteristic of rickets. At the same time the 
medullary cavity increases rapidly in size and the inner laj^ers of 
the bone become spongy. The medulla may be congested, and fat^ 
if it has formed, may be absorbed, and a modified form of osteitis 
may ensue. 

The result of these processes is that the bones do not possess so- 
lidity and cannot resist the traction of the muscles or outside pres- 
sure. The epiphyses may be displaced or bent, especially in the ribs, 
less frequently in the long bones. The long bones and the peh^c 
bones may be bent into a variety of forms. Incomplete fractures, 
are not infrequent. Complete fractures do not usually occur until 
the later stages of the disease, when the bones have become more 
solid. In the head, the cranium may be unnaturally large for the 
size of the face ; the f ontanelles and sutures may remain open ; the 
bones may be soft, porous, and hypersemic, while at their edges 
there may be rough, bony projections beneath the pericranium. 
Sometimes, especially in the occipital bone, there are rounded de- 
fects in the bone, filled only with a fibrous membrane ; this consti- 
tutes one of the forms of so-called craniotahes. 

It does not fall within the scope of this work to describe the vari- 
ous deformities which may occur as a result of this disease. The 
familiar pigeon breast ; the rows of knobs along the sides of the 
chest from bending and dilatation of the ribs at the point of junction 
of cartilage and bone ; the knock-knee, bow-legs, spinal curvatures, 
etc., may all be the result of rachitic weakening of the bones. 



^50 THE BONES. 

After a time the rachitic process may stop and the bones take on 
a more normal character. The porous bone tissue becomes compact 
.and even unnaturally dense ; the swellings at the epiphyses disap- 
pear ; many of the deformed bones may become of a normal shape. 
In severe cases, however, the deformities continue through life ; es- 
pecially is there a cessation of the growth of the bones in their long 
.axis, so that the persons affected are dwarfed. 

The disease may have an acute or a chronic character. The 
acute form begins usually during the first six months of life. The 
children are apt to suffer from vomiting, diarrhoea, profuse sweat- 
ing, chronic bronchitis and pneumonia, general ansemia, and wast- 
ing. They either die or the rachitic process is gradually developed. 
The chronic form is seen in older children, and often in those appa- 
rently healthy. The changes in the bones may take place without 
any constitutional symptoms, though there is often catarrhal bron- 
chitis, pneumonia, and ansemia. 

OSTEOMALACIA. 

This lesion consists in the softening of fully formed hard bone 
tissue by the removal of its inorganic salts. It is to be clearly distin- 
guished from rickets, whose lesions are due to a faulty development 
of bone, although in certain external characters the two diseases 
sometimes present considerable similarity. Osteomalacia usually 
occurs in adults, most frequently in females during pregnancy and 
after parturition ; more rarely it occurs in males, and in females un- 
, associated with the above conditions. Its cause is not known. 

Microscopical examination shows that the decalcification occurs 
first in the periphery of the Haversian canals and in the inner layers 
of the walls of the marrow spaces. As the salts of lime are removed 
the basement substance at first remains as a finely fibrillated mate- 
rial, still preserving the original lamellation. The bone cells may be 
changed in shape or degenerated. After a time the decalcified tissue 
may disintegrate and be absorbed, and its place occupied by new- 
formed marrow or granulation tissue. As the disease goes on the 
marrow tissue is congested and red, the fat absorbed, and there is a 
great accumulation of small spheroidal cells ; or the marrow may 
assume a gelatinous appearance. The decalcification and absorption 
of the bone from within may proceed so far that the bony substance 
in the cancellous tissue almost entirely disappears, and the compact 
bone is reduced to a thin, soft, decalcified tissue. The disease is not 
always continuously progressive, but may be subject to temporary 
cessation. 

As a result of this softened condition of the bones, the weight 
•of the body and the actions of the muscles may induce a series of 



THE BONES. 651 

•deformities which are sometimes excessive : curvatures of the spine, 
complete and incomplete fractures of the bones, distortions of the 
pelvis, sternum, etc. There is a tendency in this disease to a general 
involvement of the bones, but the changes are sometimes confined 
to single bones or groups of bones. The cranium is rarely much 
affected. 

ALTERATIONS OF THE BONE MARROW IN LEUKAEMIA AND AN.EMIA. 

In certain forms of leukaemia the marrow of the bones is very 
markedly altered. The change consists mainly in an accumulation 
in the marrow tissue of spheroidal cells, often in a condition of fatty 
degeneration, which lie in the meshes of reticular connective tissue 
and in and along the walls of the blood vessels. There may also be 
absorption of the fat, and sometimes enlargement of the marrow 
€avity from absorption of the bone. These alterations seem to be 
primarily due to an hyperplasia of the marrow cells. The new cells 
which accumulate in the marrow under these conditions are of vari- 
ous forms. Most characteristic are colorless, spheroidal cells which 
considerably resemble the large lymphocytes of normal blood (see 
page 65). But they are usually larger, though varying much in 
size, have one large, often vesicular nucleus staining less strongly 
than the lymphocyte nuclei, while the protoplasm usually contains 
neutrophile granules (page 6Q). These cells are called myelocytes. 
In addition to these the marrow may contain, mingled with, its usual 
elements, nucleated red blood cells, spheroidal cells containing red 
blood cells, and not infrequently considerable numbers of small octa- 
hedral crystals (called Charcot's crystals). 

The degree to which this accumulation of cells occurs varies much 
in different cases, and the gross appearances of the marrow are con- 
sequently very variable. In some cases the marrow is soft and has 
a uniform red appearance, or it is variously mottled with gray and 
red. Occasionally circumscribed haemorrhages are seen. In another 
class of cases, in which the cell accumulation is more excessive, the 
marrow may be gray, grayish-yellow, or puriform in appearance. 

These changes may occur in the central marrow cavity, as well as 
in the marrow spaces of the spongy bone. They may be present in 
several or many of the bones. They are usually accompanied by 
analogous changes in the spleen and lymph nodes. 

In certain cases of acute and chronic anceniia, particularly in the 
pernicious and progressive varieties, the marrow, especially of the 
larger long bones, may lose its yellow color from absorption of the 
fat, and become red. Microscopical examination of the marrow under 
these conditions may show myelocytes and sometimes an abundance 
of developing nucleated red blood cells and Charcot's crystals. 



652 THE BONES. 

In many of the acute infectious diseases, typhus and typhoid 
fever, ulcerative endocarditis, recurrent fever, etc., the bone marrow 
has been found hypersemic and containing myelocytes. 

All of these lesions of the marrow, although our knowledge of 
them is still very incomplete, together with what is known of the 
physiological functions of the marrow, point to a close relationship 
between the marrow and the spleen and lymph nodes as blood-pro- 
ducing organs.^ 

ATROPHY. 

In old age or in senile conditions the bones may become atrophied 
by the absorption of the hard tissue ; the medullary spaces are en- 
larged, the marrow tissue contains less fat and is often gelatinous in 
appearance. As the result of the lack of use, or from any cause 
which interferes with the nutrition of the bone, such as paralysis of 
the muscles or diseases of the joints, the bones may atrophy. In 
connection with atrophy there may be an ossifying periostitis, which 
results in making the bone look even larger than normal. Many of the 
conditions commonly called atrophy, such as the erosions of bones f rom 
tumors, etc., pressing upon them, are really due to a rarefying osteitis. 

The bones, sometimes as the result of atrophy and sometimes from, 
causes which we do not understand, are unusually brittle and liable 
to fracture. This disposition is sometimes hereditary. 

TUMORS. 

Tumors of the bone may involve either the periosteum, the com- 
pact bone, or the medulla, or, as is more frequently the case, two or 
more of these structures are involved at once. Tumors of the bone 
are usually accompanied by various secondary and sometimes very 
marked alterations of the bone tissue, osteo-porosis, osteo-sclerosis, 
ossifying periostitis, etc. The new growths are very apt to undergo 
calcification and ossification. 

Fibromata may grow either from the periosteum or medulla. 
Their most common seat is in the periosteum of the bones of the head 
and face. They are apt to form polypoid tumors projecting into the 
posterior nares, pharynx, mouth, and antrum of Highmore. Central 
fibromata, i.e., those growing from the medulla, are rare. They 
usually occur in the lower jaw, but have been found in the ends of 
the long bones, the phalanges of the fingers, and the vertebrse. The 
fibromata may calcify or ossify, contain cysts, and not infrequently 
occur in combination with sarcoma. 

Myxomata are of occasional occurrence in bone. 

' The literature of the researches on the diseases of the spleen, which are important 
in this connection, may be found in part in OrtKs " Lehrbuch der speciellen patholo^ 
gischen Anatomie," Berlin, 1883, erste Lieferung, p. 119 et seq. 



!^'-> 



THE BONES. Co/ 

Osteomata. — New formations of bone as a result of inflammatory 
processes are, as we have already seen, of frequent occurrence in 
bone, and although not, strictly speaking, tumors, some of their 
forms are very closely allied to them, and they may therefore be con- 
veniently mentioned here. N^ew growths of bone which arise from 
the surfaces are called exostoses or enostoses, according to their 
origin from the external surface or interior of the bone. They may 
contain all the constituents of normal bone : bone, medulla, vessels, 
periosteum, and cartilage. The new bone may be compact and like 
ivory, or spongy, or contain large cavities filled with marrow. 

The shape of exostoses varies greatly ; they may be in the form 
of sharp, narrow spiculse and processes, and, occurring in connection 
with periostitis, are called osteophytes. They may be polypoid in 
shape or form rounded tumors with a broad base. They may form a 
general enlargement of the bone, with much roughening of the sur- 
face ; this condition is often called hyperostosis. 

The bone beneath these new growths may Ije normal, or sclerosed, 
or rarefied, or the medullary cavity of the bone may communicate 
with that of the exostosis. Exostoses are usually developed from the 
periosteum, sometimes in the insertion of tendons and ligaments. 
They are very frequently multiple and may occur at all ages, even 
during uterine life. 

Enostoses are developed in the interior of bones from the medulla. 
They may increase in size, with absorption of the surrounding bone, 
until they project from the surface like exostoses. Their most fre- 
quent situation is in the bones of the cranium and face. 

Chondromata. — These tumors may be single or multiple, and 
most frequently grow from the interior of the bone, but sometimes 
from the periosteum. They are prone to form various combinations 
with other forms of tumors, as fibroma, myxoma, sarcoma, etc. 
They are frequently congenital, and are most common in young 
people. They occur most f ^-equentl}^ in the bones of the hand and foot. 

There is a form of chondroma, called osteoid chondroma, which 
develops beneath the periosteum, most frequently in the femur and 
tibia near the knee joint, forming a club-shaped enlargement of the 
bone. The characteristics of the tissue composing these tumors are 
that it resembles somewhat the immature bone tissue which is seen 
beneath the periosteum in developing bone. It difi:ers from carti- 
lage in the irregular shape of its cells, in the fibrillation and density 
of the basement substance, and in its c'eneral vascularitv. On the 
other hand, it has not the inorganic contents or appearance of true 
bone. It resembles considerably the callous tissue forming about 
fractures of the bones. It may, however, and most frequently does, 
become converted, in some parts of tlio tumor, into true bone. On 
57 



654 THE BOXES. 

the other hand, combinations with sarcomatous tissue are of frequent 
occuiTence (see below). 

Sarcoma. — This form of tumor is especially common in the 
bones. It grows from the inner layers of the periosteum or from 
the medulla, so that we may distinguish a periosteal and a raye- 
logeiiic sarcoma. Sometimes the tumor attacks the bone itself so 
early that it is unpossible to say whether the tumor began in the 
periosteum or in the medulla. There is also a variety which grows 
close to the outside of the periosteum and becomes connected with it 
—parosteal sarcoma. 

The periosteal sarcomata usvLSillj helong to the Tarieties fibro-, 
myxo-, chondro-, and osteo-sarcoma, more rarely to the medullary 
variety. They commence from the inner layers of the periosteum, 
pushing this membrane outward. After a time the periostemn is 
attacked and the tumor invades the surroundiag soft parts. The 
bone beneath may remain normal, or may be eroded and gradually 
disappear until the tumor is continuous with the medulla. Portions 
of the tumor may be calcified, or a growth of new bone may accom- 
pany its growth. The new bone usually takes the form of plates, or 
spiculse, radiating outward. The minute anatomy of these tumors 
is very variable. The simplest — the fibro-sarcomata — are composed 
of fusiform, round, stellate, and sometimes giant cells (myeloplaxes), 
in varying proportions, packed closely in a fibrous stroma. In the 
medullary form the stroma is diminished to a minimum and the 
round cells are most numerous. In the chondro- and myxo-sar- 
coma the basement substance mav be hvalin or mucous, and the 
cells follow the type of cartilage and mucous tissue more or less 
closely. There is a mixed form of tiunor, called osteoid sarcoma, 
which is very apt to spread and to form metastases. The growth 
consists in part of tissue corresponding to fibro-sarcoma and round- 
celled sarcoma. In addition to this there occurs, in greater or less 
quantity", immature bone tissue, called osteoid tissue, which may in 
part become calcified, the calcification usually occurring in the cen- 
tral portions, leaving a softer peripheral zone. This form of tumor is 
most apt to occur at the ends of the long bones, and may form tumors 
of large size. It is often called, on account of its tendency to spread 
and to form metastases, malignant osteoma or osteoid cancer. 

Myelogenic sarcomata commence in the medulla and may grow 
rapidly. The bone surrounding them is destroyed and they project 
as rounded tumors. Most frequently new bone is formed beneath 
the periosteum, so that the tumor is enclosed in a thin, bony shell ; 
sometimes there are also plates of bone in the tumor ; sometimes the 
periosteum is unaltered ; sometimes it is perforated and the tumor 
invades the surrounding soft parts. The tumors are frequently very 



THE BONES. ^55 

:Soft, vascular, and lisemorrhagic in parts, or may enclose cysts filled 
with tumor detritus and blood. They are usually of the spindle or 
round-celled variety, and not infrequently contain giant cells. 

The parosteal sarcomata resemble the periosteal, but they ap- 
pear to grow from the outer layers of the periosteum. They may 
be as firmly connected with the bone as the periosteal form.. The 
periosteum may remain intact between the tumor and the bone, or 
it may disappear and leave them in apposition. 

Angiomata and Aneurism of Bone. — A very large number of 
the tumors which have been described under these names are really 
sarcomata, or other tumors which happened to be very vascular. 
Some authors, indeed, are disposed to deny altogether the existence 
of real vascular tumors in bones. There are, however, reliable cases 
of cavernous angiomata growing between the periosteum and bone 
and intimately connected with the latter. Whether myelogenic an- 
.giomata occur is doubtful. There are several cases described of 
cavities filled with blood in the interior of bones, which it is difficult 
to interpret. They have mostly been found in the head of the tibia. 
They are said to have consisted of single sacs composed of thickened 
periosteum, lined with plates of bone, and filled with fluid and clot- 
ted blood. No large vessels communicated with the sacs, but their 
walls were covered with a rich vascular plexus, branches of which 
■opened into the cavity of the sac. 

Carcinomata. — Primary carcinomata are of very doubtful oc- 
currence in the bones. Most of the structures thus named have 
doubtless been sarcomata. Secondary carcinomata, on the other 
hand, as a result of metastases or local extension, are of not infre- 
quent occurrence and present various structural forms. Metastatic 
carcinomata may occur in the bones of various parts of the body at 
the same time, and are most apt to be secondary to carcinoma of the 
mamma. 

Cysts. — These most frequently occur in the maxillary bones, 
doubtless in connection with the teeth. They may be unilocular or 
multilocular, and contain clear serum or a mucous or brown fluid. 
and sometimes cholesterin. They may be lined with epithehum. 
They begin in the interior of the bone, and, as they increase in size, 
expand it until they may be covered with only a thin shell of bone. 
They may reach a large size, even as large as a child's head. 

Dermoid Cysts are occasionally found in connection with the 
bones, particularly of the skull. 

PARASITES. 

Ecliinococciis and cysticerciis are of rather rare occurrence in 
the bones ; the former is most frequently found. 



DISEASES OF THE JOIl^TS. 



For a description of the dislocations, misplacements, and injuries 
of the joints we refer to works on surgery. 

INFLAMMATION. 

Acute Arthritis. — The earlier stages of acute inflammation of 
the synovial membranes are better known from experiments on ani- 
mals than from post-mortem examinations. The first changes are 
swelling and congestion of the merabrane, with increased growth 
and desquamation of epithelium, and infiltration of the membrane 
with lymphoid cells. These conditions are soon followed by an exu- 
dation. The exudation may be a clear serum, in which epithelial 
cells, lymphoid cells, and sometimes blood will be found. Or floc- 
culi of fibrin may float in the serum, or the fibrin may be in excess 
and the serum nearly absent. Or there is an excessive production of 
lymphoid cells, and the synovial sac is filled with pus. 

In Serous Arthritis the accumulation of serum within the syno- 
vial sac is the most prominent lesion. The disease may terminate in 
recovery, or become chronic, or pass into the suppurative form. It 
may be caused by contusions, penetrating wounds, gonorrhoea, rheu- 
matism, or it may occur without evident cause. 

Sero-fibrinous Arthritis may occur under the same conditions as 
those which lead to simple serous inflammation. The fibrin may be 
present largely as fioccuh in the serunij or it may form false mem- 
branes over the surfaces of the joint. 

Purulent Arthritis may follow or be associated with the above 
forms of inflammation. The synovial membrane is thickened and 
cloudy, and there may be but a moderate amount of pus in the joint, 
and a shght degree of infiltration of the synovial membrane with pus 
cells. Under these conditions resolution may readily occur. 

In other cases the accumulation of pus in the cavity may be 
great, the synovial membrane and its surrounding tissue densely in- 
filtrated with pus cells. Under these conditions granulation tissue is 
apt to be found and the cartilages of the joints are apt to become 



DISEASES OF THE JOINTS. 657 

involved. There are swelling and proliferation or degeneration of the 
cartilage cells ; the basement substance becomes disintegrated, ulce- 
rates, and exposes the bone, in which osteitis, caries, rarefaction, 
etc. , may occur. The new-formed granulation tissue may penetrate 
the cartilage, absorbing the basement substance, and by metaplasia 
the cartilage tissue may be converted into embryonal or granulation 
tissue. The pus may break through the capsule of the joint and 
form large abscesses in the adjacent soft parts. Sometimes the in- 
flammation is not only suppurative but gangrenous and runs a 
rapidly fatal course. The synovial membrane, articular cartilages, 
and ends of the bone all undergo a rapid suppuration and gangrene. 
Pyaemia and septicaemia, small-pox, measles, scarlet fever, diphthe- 
ria, mumps, typhus fever, glanders, the puerperal condition, expo- 
sure to cold, penetrating wounds, and injuries, may all give rise to 
purulent synovitis. 

Chronic Arthritis may begin as such or it may be the result of 
previous acute inflammation. There is an increase of fluid in the 
joint. This fluid is thin and serous, or is thickened with flocculi of 
fibrin and epithelial and lymphoid cells, or is thick, syrupy, or even 
gelatinous. The synovial membrane is at first congested, its tufts 
prominent. Later it becomes thickened, sclerosed, and anaemic ; the 
epithelium is destroyed and the tufts become large and projecting. 
Prom the distention of the capsule there ma}^ be subluxations or lux- 
ations of the joint, or the capsule may be ruptured. 

Chronic Rheumatic Arthritis is most common in elderly per- 
sons, usually affecting several joints and advancing slowly and 
steadily. There is a chronic thickening of the synovial membrane 
and the fibrous tissue adjacent to it. Fluid accumulations are not 
common. The articular cartilages are apt to degenerate or ossify, 
or become softened and fibrillated, and they may disappear. The 
contracting synovial membranes and fibrous tissue render the joints 
stiff and may cause considerable deformity. N^ot infrequently fibrous 
and bony anchyloses are formed between the ends of the bones. 

Arthritis deformans. — This name has been applied to a variety 
of chronic inflammation of the joints which, combined with degene- 
ration of parts of the joint and the new formation of bone, may re- 
sult in marked deformities of the part. 

It usually occurs in elderly persons and is apt to involve several 
joints, most frequently the hip, knee, fingers, and feet. It may be 
idiopathic, or due to rheumatism or to injuries, or follow an acute 
arthritis. The capsules of the affected joints are thickened and scle- 
rosed. The synovial fluid is at first increased in quantity ; later, 
diminished and thickened. The tufts of the synovial membrane be- 
come much enlarged and vascular ; ihey may be converted into 



658 DISEASES OF THE JOINTS. 

cartilage. Soraetimes the capsule becomes ossified. The new bone- 
grows from the edge of the cartilage within the capsule and its- 
articular surface is covered with cartilage. The articular cartilages- 
are much changed. The basement substance splits into tufts, while 
the cartilage cells are increased in number. Or the basement sub- 
stance becomes fibrous ; or it is split into lamellse and the cartilage 
cells are multiplied ; or there is fatty degeneration and atrophy. 

As a result of these changes larger or smaller portions of the 
cartilage are destroyed and the bone beneath is laid bare. The ex- 
posed bone may become compact and of an ivory smoothness. The 
ends of the bones are much deformed. They are flattened and made 
broader by irregular new growths of bone, while at the same time 
they atrophy. The new growth of bone starts from the articular 
cartilages. The cartilage cells increase in number and the basement 
substance in quantity. This growth is most excessive at the edge of 
the cartilage, so that a projecting rim is formed there. This pro- 
jecting rim may ossify next the bone, and at the same time new carti- 
lage may form on its surface, so that we may find large masses of 
bone covered with cartilage. All these changes occur in various 
cojubinations and sequences, so that joints in this condition present 
the greatest variety of appearances. 

Arthritis uritica (Gouty Arthritis). — This disease is character- 
ized by the deposit of salts of uric acid in the cartilages, bones, and 
ligaments, and also in the ca^^ties of joints. The deposits may be 
in the form of stellate masses of acicular crystals in and about the 
cartilage cells or in the basement substance ; or they may be deposited 
in the fibrillar connective-tissue structures of the joint in single crys- 
tals, or in the subcutaneous tissue about the joint as white concre- 
tions. The deposits may occur in repeated attacks of the disease, 
and are accompanied by acute inflammatory changes. They may 
lead to various forms of chronic inflammation of the joints. 

Tubercidar Arthritis (Chronic Fungous Arthritis ; Strumous 
Arthritis). — This disease may commence in the joint itself, or be 
transmitted to it from a tubercular inflammation of the bone. It is 
characterized by the formation of granulation tissue containing 
tubercles, sometimes in great quantity, and usually associated with 
secondary inflammatory and degenerative changes of surrounding* 
parts. According to the prominence of one or other of these second- 
ary alterations, several forms of tubercular arthritis may be dis- 
tinguished. If there is an excessive growth of granulation tissue 
without much suppuration, this constitutes a fungous form. Some- 
times there is extensive suppuration, so that the cavity of the joint 
may be filled with pus, which may be discharged through oiDcnings 
in the skin ; or there may be more or less extensive formation of 



DISEASES OF THE JOINTS. Go9 

abscesses, or infiltration of the soft parts about the joint with pus. 
In other cases there is a predominant tendency to breaking-down of 
the new-formed tubercular tissue and of the tissues of the joint — 
ulcerative form. The cartilage basement substance may become 
split into fragments and the cells degenerate, and thus deep and de- 
structive ulcers of the cartilage be formed. Or the granulation tissue 
may work its way through the cartilage into the bone beneath, by 
absorption of the basement substance of the cartilage, with or with- 
out proliferation of its cells. Caries and necrosis of the underlying 
bone may lead to extensive destruction. Hand-in-hand with these 
alterations subperiosteal new formation of bone may occur, or sclero- 
sis of the adjacent bone tissue. There may also be a great increase 
of fibrous tissue about the joint. Tubercle bacilli may be found in 
the tubercular tissue and in the exudations. 

This disease is most common in children and young persons. The 
so-called scrofulous diathesis is said to predispose to it, but local 
injuries are frequently the predisposing factors. It is most common 
in the large joints. It may occur in connection with tubercular in- 
flammation in other parts of the body, but it is frequently quite 
local, and may remain so for a very long time or permanently, since 
general infection from tubercular arthritis is comi^aratively infre- 
quent. 

The disease always runs a very chronic course and may destroy 
the patient's life. If recovery takes place before the cartilages and 
bones are involved the joint is preserved ; but it may be stiffened, or 
even immovable, from the contraction of the new fibrous tissue 
around it. If the cartilages and bones are diseased the joint is de- 
stroyed, and either bony or fibrous anchylosis results. Sometimes 
from the change in the articulating surfaces, and the contraction of- 
the muscles and the new fibrous tissue, partial or complete disloca- 
tions are produced. 

Occasionally miliary tubercles occur in the synovial membranes 
in cases of general miliary tuberculosis, with but little accompanying 
simple inflammatory change. 

TUMORS. 

Secondary tumors of the joints as a result of local extension from 
the adjacent parts are not uncommon, and the tumors may be of 
various kinds. Primary tumors of the joints, on the contrary, are 
not very common. 

Lipoma. — A new growth of fatty tissue may begin in the other 
portions of the synovial membrane, push this inward, and project 
into the joint in a mass of tufts — lipoma arboreseons. 

Fibroma occurs as an hypertrophy of the little tufts aiul fringes 



6B0 DISEASES OF THE JOINTS. 

of the synovial membrane. In this \yay large polypoid and dendritic 
bodies are formed. The pedicles of these growths may atrophy and 
even disappear, so that the growths are left free in the cavities of the 
joints. 

Corpora aliena Articulorum (Loose Cartilages in the Joints). — 
This name is given to bodies, of various structure and origin, which 
are found free or attached by slender pedicles in the cavities of the 
joints. They are most frequently found in the knee ; next in order 
of frequency in the elbow, hips, ankle, shoulder, and maxillary joints. 
They may be single or in hundreds. Their size varies from that of 
a pin^s head to that of the patella. They are polypoid, rounded, egg- 
shaped, or almond-shaped ; their surface is smooth or faceted, or 
rough and mulberry-like. They are composed of fibrous tissue, car- 
tilage, and bone in various proportions. 

These bodies are formed in different ways. 

1. By hypertrophy of the synovial tufts and production of car- 
tilage and bone in them. 

2. More frequently by a change into cartilage of portions of the 
synovial membrane. Small, flat plates of cartilage form on the inner 
surface of the synovial membrane, and these increase in size and 
their outer layers ossify. They may remain fixed in the synovial 
membrane ; or they project and become detached from it, and they 
then appear as flattened, concave bodies composed of bone covered 
with cartilage on one side. 

3. The growth of cartilage and bone begins in the outer layers of 
the synovial membrane or in the periosteum near the joint. The new 
growth pushes the synovial membrane inward, and projects into the 
joint as a polypoid body covered with the inner layers of the synovial 
membrane. Later the membrane atrophies and the growth becomes 
free in the joint. 

4. There may be cartilaginous outgrowths from the edges of the 
articular cartilage. 

5. Rarely portions of the articular cartilages may be detached by 
violence or disease ; or fibrinous and other concretions may result 
from arthritis, or under conditions which we do not understand. 



MUSCLE. 



L.ESIONS OF VOLUNTARY STRIATED MUSCLE. 

Hcemorrhage. — This may occur as a result of mechanical injury ; 
from rupture of the fibres by convulsive contraction, as in tetanus ; 
or it may occur when the muscle fibres are degenerated, as in typhoid 
fever ; or in connection with certain general diseases, as scurvv^, 
purpura, hsemorrhagic diathesis, septicaemia, etc. The blood is usu- 
ally readily absorbed. 

Embolic Infarction of Muscles in connection with heart dis- 
ease has been described in a few cases, but it is rare. 

Wounds and Rupture. — When the muscle fibres are severed by 
wounds or rupture there is more or less degeneration of the divided 
fibres, and the wound may heal by the production of granulation tis- 
sue, which gradually becoines converted into cicatricial tissue, thus 
binding the severed parts together. In some cases there is a new 
formation of muscle fibres, which penetrate the cicatrix and establish 
muscular connection between the parts. When the wound does not 
gape, so that the severed ends are not much separated, there may be, 
it would seem, a direct re-establishment of muscular continuitv bv 
new development of muscle, without the formation of much new con- 
nective tissue. 

The exact way in which muscle fibres are regenerated is yet 
somewhat uncertain. In many cases there seems to be a prolifera- 
tion of the so-called muscle corpuscles, leading to the formation of 
elongated cells or strings of cells, Avhicli are gradually converted into 
striated muscle. In some cases the appearances would seem to in- 
dicate that connective-tissue cells may participate in the formation of 
new muscle fibres, but this is not certain. ^ 

INFLAMMATION. 

Suppurative Myositis. — In the early stages of this lesion wo 

^ For literature on muscle regeneratiou qow&wM Zahoroicski , Axcli. fiir exp. Patho- 
logic u. Pharm., 15(1. xxv., lloft. 5 uiul 0, p. 415, 1S89. 



662 MUSCLE. 

find the muscle hypersemic and oedematous, and the interstitial tis- 
sue more or less infiltrated with small spheroidal cells^ doubtless the 
result of emigration. If the inflammation becomes intense there 
may be an excessive accumulation of pus cells, either diffusely in the 
interstitial tissue or in larger and smaller masses. Hand-in-hand 
with this cell accumulation occur degenerative changes in the mus- 
cle fibres. By pressure their nutrition is interfered with and they 
undergo granular, fatty, or hyalin degeneration. They may com- 
pletely disintegrate and gangrene may occur^ so that larger and 
smaller masses of the infiltrated muscle tissue become soft, foul- 
smelling, and converted into a mass of detritus in which but little 
muscle structure can be detected, and which is intermingled with 
bacteria. In other cases there may be larger and smaller abscesses 
formed in the muscle, the muscle tissue itself either degenerating and 
disintegrating and mixing with the contents of the abscess, or being 
pressed aside and undergoing atrophy and degeneration. In some 
cases, when the formation of pus is moderate in amount, there may 
be restoration by formation of granulation tissue between the muscle 
fibres. This becomes gradually dense and firm, and leads to more or 
less atrophy of the muscle fibres by pressure. 

Acute suppurative myositis may accompany wounds ; it is very 
common in acute phlegmonous inflammations of the skin and subcu- 
taneous tissue, and often accompanies acute infectious diseases, such 
as pyaemia, erysipelas, etc. In most cases the pyogenic bacteria are 
present in the inflammatory foci. It is not infrequently seen in the 
muscles adjacent to the inflamed mucous membranes in diphtheria. 

Acute Parenchymatous Myositis. — A few cases of this disease 
have been described, in which, without lesion of the nervous system, 
certain groups of muscles, with the occurrence of fever and pain, be- 
come swollen, in some cases beset with small haemorrhages, soft, 
mottled with yellowish-white patches. Microscopically the muscle 
fibres showed granular and fatty, or in some cases waxy, degenera- 
tion. The cause of this lesion is not known. In one case the mus- 
cles of the legs were thus affected in a woman who died in the first 
week after delivery, with fever and pain in the legs, and the lesion 
was conjecturally of infectious origin.^ 

Chronic Interstitial Myositis. — In this lesion there is a new 
formation of connective tissue between the muscle fibres or bundles 
of fibres. This new tissue is sometimes very cellular, resembling 
granulation tissue, and this probably represents an early stage of the 
disease. In other cases (Fig. 296) we find dense cicatricial tissue 

^Consult Eisenlohr, Centralblatt flir Nervenlieilkunde, i., 1879; Marchand, Bres- 
lauer Aerztliche Zeitschrif t, xxi. , 1S80. 



MUSCLE. 



665 



crowding the muscle fibres apart, inducing atrophy in them, and 
sometimes causing their complete destruction. This lesion, which is 
the analogue of chronic interstitial inflammation of the internal 
organs, may occur in muscles which are adjacent to other parts which 
are the seat of chronic inflammatory processes. It may occur in. 
muscles which are not used. The new formation of connective tissue 
would in some cases seem to be secondary to atrophy of the muscle 
fibres. 

Myositis ossificans. — Under conditions and for reasons which 
we do not understand, there occasionally occurs, usually in young 
persons, a new formation of bone tissue in the interstitial tissue of 



^^^^-^^^^^^^^^""^^^i 



















-\vi 



Fig. 296.— Chronic Interstitial Myositis. 



The connective tissue is dense in texture, and the muscle fibres are atrophied and partialis 
destroyed. 



muscles, in the tendons, ligaments, fasciae, and aponeuroses. This 
sometimes apparently starts as outgrowths from the periosteum, 
sometimes not. The bone formations are apt to commence about the 
neck and back, and may become very widespread over the body. So 
far as the muscles are concerned, there is usually an increase of con- 
nective tissue between the fibres and bundles, in which new bono is 
formed, usually in elongated and sometimes in spicula-liko masses. 
The muscle fibres under i2:o secondarily a Q'reater or less deu'reo of at- 
rophy or degeneration. There may be fatty infiltration botwoeu the 



664 MUSCLE. 

fibres, and various deformities are produced by the shortening and 
progressive immobihty of the affected parts. ' 

While the above disease is a progressive and frequently a general 
one, there may be new formation of bone in muscle as a result of pro- 
longed or repeated mechanical irritation. Thus in the adductors of 
the thigh in persons who are constantly in the saddle, or in the del- 
toid muscle of soldiers who strike this part with their weapons in 
drill, there may be a formation of bone. 

Gummata and occasionally tubercles occur in the connective tis- 
sue of muscle. 

DEGENERATIVE CHANGES IN THE MUSCLES. 

Simple AU^ophy. — This may occur in old age, in prolonged ex- 
hausting diseases, or as a result of pressure from a foreign body. 



^^felp'l?. 



;:riil;■^^y?;v■;■>;■.;;•■■;i;■:■',-,-:->i:^^^■:i^,\2J'2■^^4^^^^ 



?^sSH^^=5iiiisiisia?? 



.^^__^^^^^^^^. 

«*?■; 









Fig. 297. — Progressive Muscular Atrophy (Soleus muscle, locgitudinal section). 

a, atrophied muscle fibre; 6, degenerated muscle fibre; c, interstitial tissue; d, clusters of pro- 
liferated muscle nuclei. 

tumors, etc. The muscle fibres grow narrower, the degree of narrow- 
ing frequently varying considerably in different parts. They usually 
retain the striations, but these may be obscured by degenerative 
changes. The sarcolemma may become thickened, and there may 
be a considerable increase in connective tissue between the muscle 
fibres and bundles. 

Progressive Muscular Atrophy. — This lesion consists essentially 
in a combination of simple or degenerative atrophy of the muscle 
fibres with chronic interstitial inflammation, and is sometimes associ- 
ated with proliferative changes in the muscle nuclei. In the earher 

^ The literature of Myositis ossificans may be found, together with a description of 
some interesting cases, in an article by Mays in Virch. Archiv, Bd. Ixxiv., p. 145. 



MUSCLE. 



fjfjo 



stages of the disease the muscles may be pale and soft, but exhibit 
otherwise to the naked eye but little alteration. Gradually, however, 
the muscle substance becomes replaced by connective tissue, so that 
in marked and advanced cases the muscles are converted into fibrous 
bands or cords, whose cicatricial contraction may induce great de- 
formities. 

Microscopical examination shows in the early stages of the disease 
a proliferation of cells in the interstitial tissue, so that this may have 
the appearance of granulation or embryonal tissue ; also in some 
cases marked proliferative changes in the muscle nuclei (Fig. 297),. 




FiQ. 298.— Progressive Muscular Atrophy (Soleiis muscle, transverse section), 
a, increased interstitial tissue; b, nearly normal muscle fibres; c, degenerated muscle fibres; 
d, atrophied muscle fibres; e, clusters of proliferated muscle nuclei. 

leading to the formation of new cells which may more or less replace 
the contractile substance within the sarcolemma. The new inter- 
stitial tissue increases in quantity and grows denser, and may crowd 
the muscle fibres apart (Fig. 208). The walls of the blood vessels 
may also become thickened. Hand-in-hand with these interstitial 
alterations the atrophy of the muscle fibres proceeds. These may 
simply grow narrower, retaining their striations ; or they may split 
up into longitudinal fibrillin, or transversely into discoid masses, and 
in this condition disappear. In other cases a certain amount of 
fatty or hyalin degeneration may be present. These degenerative and 



s. 



666 



MUSCLE. 



proliferative changes do not, as a rule, occur uniformly in the affected 
muscles, but some parts are affected earher and more markedly than 
others. The atrophied muscle may be replaced by fat. 

Progressive muscular atrophy is apt to commence in the small 
muscles of the extremities, in many cases in the muscles of the ball 
of the thumb. It may commence in the muscles of the shoulder, 
the arms, or the back. It may have a continuous extension, or it 
may jump single muscles or groups of muscles. Death may be in- 
duced by the affection of the muscles of respiration or deglutition. 

The causes of this lesion are in many cases unknown, and there 




is considerable lack of unanimity of opinion as to whether it is pri- 
marily a disease of the muscles or of the nervous system. In a 
considerable proportion of cases the muscle lesion is associated with 
atrophy of the ganglion cells in the anterior cornua of the spinal 
cord and the development of connective tissue about thenir In 
other cases these changes in the cord may apparently be absent. 

It is sometimes accompanied by atrophy of the nerves which are 
distributed to the muscles, and atrophy of the anterior roots has 
been described. 

It is probable that there are several varieties of progressive mus- 
cular atrophy, which our present knowledge does not enable us to 



MUSCLE. 6fJ7 

clearly distinguish. Muscular atrophy in some cases follows over- 
straining of groups of muscles, or injuries, and may occur as one 
of the sequela3 of typhoid fever and diphtheria. 

Atrophia Musculorum lipouiatosa (Pseudo-hypertrophy of the 
Muscles). — In some cases, hand-in-hand with the production of new 
connective tissue in the muscles and the atrophy of the muscle 
fibres, or after these changes have made considerable progress, there 
occurs a development of fat tissue between the fibres (Fig. 299) which 
may prevent any apparent diminution in the size of the muscles, or 
in some cases may even give them a great increase in size. This condi- 
tion is of most frequent occurrence in children, and is most apt to 
aj^pear in the gastrocnemii muscles. In the upper extremities the 
deltoid and triceps are most frequently involved. The lesion may be 
symmetrical, affecting similar muscles on both sides of the body, or 
it may be unilateral. Parts of muscle bellies may be affected. 

The cause of this form of atrophy is not definitely known. Vari- 
ous lesions of the spinal cord have been described as occurring with 
it ; but, in many cases at least, alterations of the nervous system 
cannot be detected. The writer has described a case ^ in which this 
lesion was marked in the gastrocnemii in connection with multiple 
false neuromata.^ 

Fatty Degeneration, with greater or less destruction of the mus- 
cles, may commence with a simple swelling and fine granulation of 
the fibres. As the process goes on, smaller and larger fat droplets 
appear in the contractile substance, which loses its striations and 
l^ecomes friable, and may be entirely destroyed, leaving within the 
sarcolemma a mass of fatty detritus which may finally be absorbed 
and disappear. This alteration may occur in acute parencliAiiiatous 
myositis in connection with various forms of atrophy, in prolonged 
exhausting diseases, and in phosphorus poisoning. 

Hyalin Degeneration. — Under a variety of conditions the mus- 
cle fibres undergo a peculiar series of changes, leading to their con- 
version into a translucent, highly refractile material, somewhat re- 
sembling amyloid but not giving its micro-chemical reactions, and 
apparently more nearly allied to the material produced in the so- 
called hyalin degeneration. The lesion in the muscle which we 
are considering is commonly called ivaxy degeneration, from the 
peculiar appearance which the muscles present. "When the lesion is 
far advanced and extensive the muscles are brittle and have a gray- 

^ Prudden, American Journal of IMedical Sciences, July, 18S0,- p. 134. 

'^ For bibliography of muscular atrophy consult Friedreich, '"VchQV progressive 
Muskelatrophie," etc., Berlin, 1873 ; also " Dictiounaire eucyclopodique des Sciences 
medicales," 2 ser., 1., x. ; or Eulcnberg's " Real-Eucyclopadie der gesanimteu lleil- 
kundc," article by Pick on Muskelatrophie. 



668 



MUSCLE. 



ish-yellow, translucent appearance. Microscopical examination of 
various stages of hyalin degeneration of muscle shows that the con- 
tractile substance of the fibres becomes at first swollen and granular, 
and gradually converted into hyalin material which may present 
the outlines of the swollen fibres, but is more frequently broken into 
larger and smaller shapeless clumps (Fig. 300), which may disin- 
tegrate and finally be absorbed. Hand-in-hand with these changes 
there usually occurs an increase in the interfibrillar connective tissue, 
and in certain cases there may be a proliferation of the muscle nuclei 
and a new formation of variously shaped cells within the sarco- 
lemma which leads to the regeneration of the fibres. As a result of 
the brittleness of the degenerated muscles they are apt to rupture, 
and in this way haemorrhage may occur. 

This form of degeneration may occur in progressive muscular 
atrophy, in variola, cerebro-spinal meningitis, trichinosis, in connec- 
tion with inflammation, injuries, freezing, etc. It is, however, most 













Fig. 300 —Hyalin Degeneration (so-called Waxy Degeneration) of Abdominal Muscle in 

Typhoid Fever. 

marked and frequent in typhoid fever. In this disease the rectus 
abdominis and the adductors of the thigh are most frequently 
affected. 

Experimental investigations have shown that, under certain con- 
ditions, very similar appearances may be produced in the muscles by 
post-mortem changes. It is not unlikely that a variety of changes 
are at present included under the name waxy or hyalin degeneration 
of the muscles. ' 

Hypertrophy of Muscle. — True hypertrophy of muscle as a 
pathological condition is rare, but it has been described in a few 
cases. It is usually confined to circumscribed groups of muscles. 
On microscopical examination the diameter of the fibres is increased, 
sometimes considerably, though not uniformly. The transverse stri- 



^ Consult Zenker, " Ueber die Veranderung der willklirlichen Muskeln in Typhus 
abdominalis," Leipzig, 1864; also WeiJil, "Exp, Unters. ti. d. wachsartige Degene- 
ration der quergestr. Muskeln," Virch, Arch., Bd. Ixi., p. 258, 1874. 



MUSCLE. 669 

ation is unaltered and the muscle nuclei are in some cases enlarged. 
The cause of the change is unknown. 

TUMORS. 

The tumors of the muscles usually develop in the connective 
tissue. Fibroma, chondroma, lipoma, myxoma, sarcoma may 
occur as primary tumors. Carcinomata and sarcomata may occur 
secondarily in the muscles as a result of local extension from adjacent 
parts. The muscle fibres are, as a rule, only secondarily affected by 
pressure, etc. , in tumors of the muscles, but there exist observations 
which point to the possibility of a proliferation of the muscle nuclei 
and the new formation from them of cells which may take part in 
the growth of the tumor. 

PARASITES. 

The Trichina sjnralis is the most common parasite in the mus- 
cles. 

Cysticercus celluloste and Echinococcus occasionally occur. 

58 



PART ly. 



THE LESIOI^S EOUJSTD 



IN 



THE GEISTEEAL DISEASES, 



IN 



POISOTvTIlSrG, 



AND IN 



VIOLEIsTT DEATHS. 



DISEASES OHAEACTEPJZED BY ALTEEA- 
TIOIsTS IlSr THE COMPOSITIOX OE 

THE BLOOD. 



There is a group of diseases in which the essential lesion seems to 
be an alteration in the composition of the blood, although in some 
members of the group other lesions are also present. This group 
embraces Chlorosis, Pernicious Ansemia, Addison^s Disease, Leu- 
kaemia, and Pseudo-leukaemia. 

CHLOROSIS. 

In many cases of chlorosis the only lesion is the change in the 
composition of the blood. 

The red blood globules may contain less haemoglobin than normal 
and the number of red blood cells be diminished. There are present 
red blood cells, some of which are larger and some smaller than the 
normal cells. There may be irregular-shaped red blood cells — poiki- 
locytes (see page 64). 

In some cases there is also present a congenital smallness of the 
aorta. 

PERNICIOUS AN.^MIA. 

In this disease the relative number of the red blood cells may be 
greatly diminished, and these may vary greatly in size and form (see 
page 04:). Nucleated red blood cells are common. There is usually 
in the blood a relatively large haemoglobin content, though the num- 
ber of the red blood cells be diminished. The luimber of leucocytes 
may be increased, or remain in normal })roportion, or be diminished. 
The mononuclear leucocytes are apt to be more abundant than in 
normal blood. 

Haemorrhages are common in various parts of the body. The 
heart muscle and liver may be fatty. There may be fatty degenera- 
tion in the walls of the arteries. Atrophy of the gastric mucous 
membrane is not infrequent. 



674 DISEASES CHARACTERIZED BY ALTERATIONS 



ADDISON'S DISEASE. 

This name is applied to a disease characterized by a peculiar pig- 
mentation of the skin and by certain changes in the suprarenal cap- 
sules. The patients become very anaemic, but are not emaciated. 
They suffer from cerebral symptoms, great prostration, syncope, and 
derangements of the functions of the stomach and intestines. 

The pigmentation of the skin is the symptom which has espe- 
cially attracted attention. The change in color usually begins and 
becomes most marked in those parts of the skin which are not cov- 
ered by the clothing or are naturally darker colored. The rest of 
the skin afterward changes color, but not uniformly, white patches 
being left. The color is at first a light yellow or brown ; this be- 
comes darker until it is of a dark greenish, grayish, or blackish 
brown. The mucous membrane of the tongue, lips, and gums may 
be pigmented in the same way. 

Under the name of Addison^s disease different observers have de- 
.^cribed cases in which the symptoms and bronzed skin existed with- 
out disease of the suprarenal capsules ; cases in which the bronzed 
skin was the only lesion ; and cases in which the suprarenal capsules 
were diseased without symptoms or bronzed skin. 

We hardly know as yet what are really the characteristic lesions 
of the disease. 

The Skin. — The discoloration of the skin is due to deposit of yel- 
lowish-brown pigment in the deeper layers of the epidermis, espe- 
cially in the layer covering the papillae, and less constantly in the 
connective tissue of the cutis. 

The Brain. — Pigmentation of the gray matter, acute meningi- 
tis, chronic meningitis, and distention of the ventricles with serum 
have been observed. 

The Heart. — The muscular fibres may be the seat of fatty de- 
generation. 

The Sympathetic Nerves may show a variety of changes appa- 
rently due to chronic inflammation, especially the nerves which are 
in contact with the suprarenal capsules. Various changes in the 
semilunar ganglia have been described. 

The Suprarenal Capsules. — The most common lesion of these 
bodies is a tubercular inflammation resembling that which occurs in 
the lymphatic glands. 

The suprarenal capsules are large, hard, and nodular ; less fre- 
quently of normal size or smaller than normal. On section they are 
found to contain cheesy masses surrounded by zones of gray, semi- 
translucent tissue. Later the cheesy masses may become calcified or 



IN THE COMPOSITION OF THE BLOOD. 675 

they may soften and break down. The grayish zones are composed 
of tubercle tissue, granulation tissue, and connective tissue. 

Other cases have been described in which the suprarenal capsules 
were the seat of carcinoma or of fatty or waxy degeneration. The 
suprarenal capsules in some cases appear normal or they may be 
atrophied. 

LEUKEMIA (LEUCOCYTH^MIA). 

This disease is characterized by a persistent and progressive in- 
crease in the number of white blood cells in the blood, accompanied 
by alterations of varying amount in the spleen, lymph nodes, and 
bone marrow. Sometimes one, sometimes another of these organs is 
especially involved, and so varieties of leukaemia are sometimes des- 
ignated. Thus when the bone marrow and spleen are most mark- 
edly involved the condition is called lineo-medullary leukcemia ; if 
there is a special involvement of the bone marrow it is called myelo- 
genous leukcemia ; while lymphatic leukcemia calls attention to 
the prominence of the lymph node lesion. Not infrequently other 
internal organs, lungs, liver, kidneys, etc., are more or less densely 
infiltrated with leucocytes, either diffusely or in nodular form. The 
lymphatic tissue of the gastro-intestinal canal may be in a condition 
of hyperplasia. 

Ecchymoses in the serous and mucous membranes, or severe 
haemorrhages on slight provocation, and fatty degeneration of the 
heart and kidneys, frequently complicate leukaemia. Aside from va- 
rious other foreign chemical substances which may exist in the blood 
in leukaemia, there are very frequently found in the blood, marrow, 
spleen, liver, etc., after death, elongated octahedral crj'stals, called 
Charcot's crystals, which are believed to be formed by a combina- 
tion of phosphoric acid with some organic base. 

For a detailed description of the lesions of the different parts of 
the body in leukaemia see chapters on Blood, Spleen, Lymph Xodes, 
Bones, etc. It does not fall within the scope of this work to con- 
sider the various theories as to the probable causes of this disease, 
which is very obscure and but little understood. 

PSEUDO-LEUKEMIA (HODGKIN'S DISEASE). 

This disease is characterized by hyperplasia of the lymph nodes 
and nodules, with an occasional but b}' no means constant involve- 
ment of the spleen, liver, and bone marrow, somewhat similar to that 
in leukj^mia. Anaemia is a very constant factor in this disease, but 
the characteristic increase in leucocytes of leuki\?mia is wanting. 



SOOEB1TTLTS-PITEPITEA-H.EMATOPHILIA. 



SCORBUTUS (SCURVY). 



This disease appears to result from imperfect nutrition under con- 
ditions which cannot be considered here, and whose immediate cause 
we do not understand. The lesions are variable, the most prominent 
being extravasation of blood in the skin, subcutaneous tissue, and 
muscles ; swelling and ulceration of the gums. Small and some- 
times extensive hsemorrhages are apt to occur in the mucous mem- 
branes and on serous surfaces. Small ulcers may form in the mu- 
cous membranes. Fatty degeneration of the heart, liver, and 
kidneys is not uncommon. The spleen may be large and soft. No 
constant characteristic changes have been discovered, either in the 
blood vessels or the blood, which would satisfactorily account for the 
extravasations and other lesions. 

The body is apt to decompose early. The skin may be mottled 
with small and large purple, blue, brown, or blackish spots produced 
by degenerative changes in the extravasated blood in the cutis. 
Sometimes ulcers are produced by the perforation of effused blood on 
to the surface. 

The joints may be inflamed, may contain serum or blood. Rarely 
the hsemorrhages are followed by destruction of the cartilages and 
ends of the bones. 

Very rarely there is hsemorrhage between the periosteum and 
bone, and in the bone itself, producing softening and destruction of 
the bone, and separation of the epiphyses. The sternal ends of the 
ribs are the most frequent seat of this change. 

That some forms or phases of scorbutus are of mfectious nature 
is not improbable, but definite data in this direction are wanting. 

PURPURA H^MORRHAaiCA (MORBUS MACULOSUS). 

This disease is characterized by the occurrence of ecchymoses in 
the skin, mucous and serous membranes. Hsemorrhages, particu- 
larly from the mucous membranes, may be very severe and even 



SCORBUTUS — PURPURA — H/KMATOPHILIA. 077 

fatal. The cause of the disease is unknown. A few cases have 
been described under this name in which the characteristic ecchy- 
moses were associated with the pyogenic bacteria, representing, it 
would seem, a phase of pyaemia. Whether any considerable num- 
ber of cases of this disease are associated with bacteria we do not 
yet know. 

H^MATOPHILIA (HEMORRHAGIC DIATHESIS). 

This disease consists in a liability to haemorrhage on the slightest 
provocation, and is dependent upon some constitutional peculiarity 
which is unknown to us. It is frequently hereditary. An unusual 
thinness of the intima of the arteries has been noticed in some cases, 
and other changes have been described ; but there are no constant 
lesions associated with hcemorrhages, as yet discovered, which would 
satisfactorily explain their occurrence. The haemorrhages may be 
traumatic in origin, or they may occur spontaneously from the mu- 
cous membranes. 



GOUT. 



The characteristic lesion of gout is the deposit of urate of soda in 
the articular cartilages, the ligaments of the joints, the ears, and the 
eyelids. 

The most frequent situation is the metatarso-phalangeal joint of 
the great toe. The cartilage may be infiltrated or encrusted with the 
deposit. 

A very important feature of gout is that patients with the gouty 
diathesis are especially liable to derangements of digestion and to 
certain chronic inflammations, such as chronic inflammation of the 
arteries, chronic bronchitis, and chronic nephritis. 



DIABETES. 



It would be expected that so common and well marked a disease 
as saccharin diabetes should be characterized by definite lesions, but 
this is not the case. The changes which we find after death are ac- 
cidental or the results of the disease. No characteristic lesions have 
yet been discovered. 

The Brain may appear to be entirely normal ; it may be con- 
gested ; there may be an increase of serum ; the convolutions may 
be shrunken ; there may be meningitis ; there may be dilatation of 
the blood vessels, small extravasations of blood around the vessels, 
enlargement of the perivascular spaces, and alterations in the peri- 
vascular sheaths and nervous matter bounding the cavities : there 
may be tumors at the base of the brain. 

The Spinal Coixl may present dilatation of the blood vessels ; di- 
latation of the central canal ; changes in the gray matter of the an- 
terior cornua. 

The Lungs. — There may be pleurisy, bronchitis, broncho-pneu- 
monia, lobar pneumonia, gangrene of the lung, chronic pulmonary 
phthisis. 

The Heart is often small ; there may be chronic endocarditis. 

The Stomach and Intestines. — The stomach may be dilated, its 
walls may be thickened, there may be hsemorrhagic erosions of the 
mucous membrane. In the intestines there may be tubercular ulcers 
or enteritis. 

The Liver and the Spleen show no marked changes. 

The Pancreas may be atrophied ; it ma}" contain abscesses. 

The Kidneys may be enlarged ; they may be the seat of paren- 
chymatous degeneration or diffuse nephritis : there may be glyco- 
genic degeneration of the epithelium of Henle's loops. 

The Blood. — In a few cases fat has been found in the blood, and 
fat emboli in the vessels of the lungs. 



SU]^STEOKE (INSOLATIONS'). 



During the hot summer months cases of sunstroke are of frequent 
occurrence in New York. The persons affected are, for the most 
part, adult male laborers, usually of intemperate habits. 

It is necessary to separate from the cases of sunstroke proper, 
when the patient is attacked w^hile exposed to the heat of the sun, 
the cases of exhaustion from heat and fatigue, which may occur as 
well in the house. 

The patients who are seriously affected by sunstroke exhibit, dur- 
ing life, an intense heat of the skin, convulsions, and coma. Death 
in many cases soon ensues. In other cases the symptoms are more 
protracted. 

After death, decomposition sets in very early, owing to the state 
of the weather. In autopsies which we have made within two hours 
after death the increased heat of the skin was still maintained. 

The Brain and its membranes were in some cases congested, in 
others not. Sometimes there was an increased amount of serum be- 
neath the pia mater ; sometimes there were small and thin extrava- 
sations of blood beneath the j)ia mater and between the pia and dura 
mater. 

In the other ^"iscera there were no lesions except those due to the 
condition of coma existing before death. The lungs and kidneys 
were frequently congested. 

In the cases in which cerebral symptoms are protracted for a num- 
ber of days the lesions of meningitis have been found after death. 

Attention has been called by Dr. H. C. Wood, Jr., to the rigid 
condition of the wall of the heart after death, but this rigidity is cer- 
tainly not present in all cases. 

According to Cramer,^ persons surviving for some time the first 
severe effects of the heat may suffer important alterations in certain 
nerve fibres of the brain. 

^ Cramer, Centralblatt fur allg. Path., etc., March 15th, 1890. 



DEATH FEOM BUE^TIXG. 



Death may be caused by the inspiration of smoke and flame ; by 
drinking of hot fluids ; by the direct contact of flame or hot sub- 
stances with the external surface of body. It may be due to the di- 
rect effect of the agents, to secondary affections of the viscera, or to 
the exhaustion produced by long-continued inflammation and sup- 
puration. 

Sudden death may occur after extensive burnings of the skin. ' 

The entire body may be burned to a coal or completely roasted, or 
only a larger or smaller area of the skin be burned. 

We find the burned skin divested of epidermis and presenting a 
peculiar red, hard, parchment-like appearance. If the patient has 
lived some time, this is replaced by a suppurating surface. Or there 
are small, bladder-like elevations of the epidermis. The base of 
these blisters is red and they are surrounded by a red zone, or sup- 
puration may have commenced. 

These appearances cannot be produced by heat applied to the 
skin after death. 

The Brain may be congested, oedematous, or softened. ^lore 
frequently it is normal. 

The Larynx cind Trachea may be congested and the seat of 
croupous inflammation. There may be oedema of the glottis. 

77? e X?/j^(/5 may be congested and oedematous, or hepatized, or 
the seat of pysemic infarctions. There may be pleurisy. 

In^mjmvcdion oi i\\e peritoneiim \^ not very infrequent. There 
may be swelling of the solitary and agminated nodules of the small 
intestine. 

The duodenum may be the seat of perforating ulcers, and the mu- 
cous membrane of the entire gastro-intestinal canal may be con- 
gested. The Liver, Spleen, cind Kidneys ms.ry he the seat o^ pa- 
renchymatous degeneration or of pynemic infarctions. 

'For literature on sudden death following severe burns consult Silhrrfihtfui, 
Virch. Arch., Bd. cxix., p. 488, 1890. 



DEATH FEOM ELECTRICITY. 



Lightning. — Persons who are struck by lightning may die in- 
stantly ; or may continue for several hours comatose or delirious, and 
then either die or recover ; or they may die after some time from the 
effects of the burns and injuries received. 

The post-mortem appearances are very variable. Sometimes 
there are no marks of external violence or internal lesions. Some- 
times the clothes are burnt and torn, while the skin beneath them is 
unchanged. Usually there are marks of contusion and laceration, or 
ecchymoses, or lacerated, punctured wounds, or fractures of the bones, 
or superficial or deep burns. The track of the electric fluid may 
sometimes be marked by dark-red arborescent streaks on the skin. 
Fractures are rare. 

The internal viscera may be lacerated and disorganized from 
lightning. 

Artificial Electrical Currents. — In death from powerful artifi- 
cial electrical currents, either by accident, as in linemen and others, 
or in electrical executions, there may be local burnings of varying 
degree where the wires or electrodes come in contact with the skin. 
The clothes may be pierced with holes at the point of exit of the 
current. 

Internally there appear to be no marked or characteristic lesions, 
either gross or microscopical, in this form of death. 

Van Gieson ^ and others have observed the occasional, but not 
constant, occurrence of small hsemorrhages in the floor of the fourth 
ventricle, the significance of which is doubtful. Other petechial 
spots have been observed beneath the serous surfaces of the endo- 
cardium, pericardium, and pleura, and on the spleen. 

^ Van Oieson, "A Report of the Gross and Microscopical Examination of Six 
Cases of Death by Strong Electrical Currents." Reprint from the New York Medi- 
cal Journal, May 7th and 14th, 1892. 



I3EATII FEOM SUFFOCATTDX-ASPIITXIA. 



By suffocation we understand that condition in which air is pre- 
vented from penetrating into the lungs without direct pressure on 
the larynx or trachea. The interruption of the function of respira- 
tion which is thus brought about induces the condition known as 
asphyxia. Many deaths from drowning and strangulation take 
place in this way. 

The methods in which the supply of air may be cut off from the 
lungs are very various. The mouth and nose may be closed by the 
hand, by plasters and cloths, by wrapping up the head in cloths, by 
covering the face with earth, hay, grain, etc. Foreign bodies may 
be introduced into the mouth, pharynx, and larynx. Blood may 
pass into the trachea from an aneurism or from a wound. The glot- 
tis may be closed by inflammatory swelling. Matters which are 
vomited may lodge in the larynx. 

On the other hand, injury or disease of the medulla oblongata, or 
paralysis or spasm of the muscles of respiration from drugs, tumors 
pressing upon the air passages, or diseases of the lungs themselves, 
may induce asphyxia. 

EXTERNAL INSPECTION. 

The body should be examined for marks of violence, the cavities 
of the mouth and nose for foreign substances. 

The face may be livid and swollen or present a natural appear- 
ance. The conjunctiva may be congested and ecchymotic. There 
may be small ecchymoses on the face, neck, and chest. The mouth 
often contains froth}^ blood and mucus. The tongue may be pro- 
truded. 

INTERNAL EXAMINATION. 

71ie Biain cind its membranes may be congested, or anaMuic and 
oedematous, or unchanged. 

TJie Blood throughout the body is unusually dark-colorod and 
fluid. 



684 DEATH FROM SUFFOCATIOX — ASPHYXIA. 

The Larynx may contain foreign bodies which have produced the 
suffocation. The mucous membrane of the larynx, trachea, and 
bronchi is congested and sometimes ecchymotic. These passages 
contain frothy blood and mucus. 

The Lungs are usually congested and oedematous, but sometimes 
do not differ from their ordinary appearance. There may be small 
patches of emphysema near the surface of the lungs. Sometimes, 
especially in infants, small ecchymoses are found in the costal and 
pulmonary pleura. 

The Heart usually ]3resents its right cavities ix^ of blood, its 
left cavities empty ; but to this there are frequent exceptions. 

The Abdominal Viscera are usually congested. 

DEATH FROM STRANGULATION— HANGING. 

Strangulation is effected by the weight of the body in hanging, 
by pressure on the neck with the hands or by some other object, or 
by constriction of the neck with a cord or ligature of some kind. 
Death is usually produced by asphyxia, or by asphyxia combined 
with the effect of the cutting-off of the blood supply to the brain by 
pressure on the large vessels of the neck. In some cases of hanging, 
death ensues as a result of fracture or dislocation of the cervical ver- 
tebrae. 

EXTERNAL IXSPECTIOX. 

The face may be livid and swollen, the eyes prominent, the lips 
swollen, and the tongue protruded. These appearances are, how- 
ever, often absent. Erection of the penis, 3Jaculation of semen, and 
evacuation of faeces and urine are frequently observed. 

In most ca>ses marks are left upon the neck by the objects which 
have directly produced the strangulation. 

In cases of hanging, the mark about the neck varies considerably 
in positioii, direction, and general characters, depending upon the 
kind of ligature employed, the time of suspension, period after death 
at which the observation is made, etc. The most common mark 
left by a cord about the neck is a dry, dense, brownish furrow, 
whose breadth corresponds but in a very general way with the 
diameter of the cord. In some cases, according to Tidy and others, 
there may be no mark at all if the hanging is quickly accomplished 
with a soft ligature and the body cut down immediately after death. 
There may be abrasions and ecchymoses of the skin at the seat of 
ligature. 

In cases of strangulation by the fingers the marks on the neck 
may correspond in a general way to the shape of the fingers. 



DEATH FROM SUFFOCATION — ASPHYXIA. 085 

The application of the same forces immediately after death may 
produce the same marks as when death is induced by them. 

INTERNAL EXAMINATION. 

The Brain and its membranes may be congested, or there may 
be extravasation of blood, or there may be no abnormal appearances. 

The Neck. — In some cases there is effusion of blood beneath the 
ligature, rupture of the cervical muscles, fracture of the os hyoides 
and cartilages of the larynx, fracture and dislocation of the cervical 
vertebrae, rupture of the internal vertebral ligaments and of the inner 
and middle coats of the carotid arteries. Similar changes may be 
produced in the dead body by the use of great violence. In death 
from asphyxia the lesions are similar to those described above. In 
some cases — for example, where death has occurred from fright or 
shock — the results of post-mortem examination are entirely negative. 

DEATH FROM DROWNING. 

In examining the bodies of persons who have been drowned it is 
necessary to bear in mind a number of questions which may arise : 
Whether the person came into the water alive or dead ? How long 
a time has elapsed since death ? Whether the person committed sui- 
cide, or was drowned by accident, or was murdered ? These ques- 
tions are to be solved sometimes certainly, sometimes with proba- 
bility, sometimes not at all, by the post-mortem examination. 
Persons dying in the water, to which condition the term drowning 
is commonly applied, may die from asphyxia, from exhaustion, from 
fright or syncope, from diseases of the heart, apoplexy, injuries, etc. 
While in the majority of cases asphyxia is a predominant or impor- 
tant factor in death by drowning, the conditions under which death 
occurs are so apt to be complex that in the minority of cases only are 
the lesions of pure asphyxia found after death, while in most cases 
the bodies present the more or less well-marked lesions of asphyxia 
together with those indicative of complicating conditions. There are 
no post-mortem conditions which alone are absolutel}^ characteristic 
of drowning, and it is only by considering all the facts elicited by 
the autopsy together that any just conclusion can be arrived at. It 
should always be borne in mind, moreover, that even the most char- 
acteristic of the evidences of drowning are apt to be modified or to 
disappear as decomposition goes on. 

EXTERNAL INSPECTION. 

Post-mortejn rigidity usually sets in early, sometimes immediately 
after death. Decomposition goes on. especially in sunimer, with 
59 



686 DEATH FROM SUFFOCATION — ASPHYXIA. 

unusual rapidity in bodies which have been removed from the water. 
Frequently, but by no means constantly, the peculiar roughening of 
the skin, known as goose skin (cutis anserina), is found, but this may 
occur after death from other causes. A light, lathery froth, either 
white or blood-stained, is frequently seen about the mouth and nos- 
trils ^vithin twelve to twenty -four hours after removal of the body 
from the water, but it may be absent, and may be seen after death 
■ from other causes. After the body has lain for several hours in the 
water (twelve to twenty -four) the thick skin of the palms of the 
hands and soles of the feet may become macerated and thrown into 
coarse wrinkles, just as it may after prolonged soaking during life, 
or in a dead body thrown into the water. The penis and nipples 
may be retracted and the scrotum shrunken, but this is not constant 
nor characteristic. 

If the person has struggled in the w^ater and clutched at objects 
within his reach, there may be evidences of this in excoriations of 
the fingers or in the presence of sand, weeds, etc., under the nails or 
grasped in the hands. 

External marks of injury, bruises, etc., should be sought for, 
since persons in diving, or on being thrown into the water with homi- 
cidal intent, may have died from the violence, and not, strictly speak- 
ing, from drowning. It should also be borne in mind in such com- 
plex cases that injuries, not in themselves fatal, may, when the body 
is in the water, prove so on account of the inability of the person to 
rescue himself or gain time for recovery from the injury, and that 
then the struggle for breath may be but slight, and the more promi- 
nent signs of drowning but little marked. 

INTERNAL EXAMINATION. 

The Brain. — Congestion of the brain and its membranes is found 
only in a small proportion of cases. 

The Blood, when death occurs from asphyxia, is usually fluid 
throughout the body and of a dark color, as in asphyxia from other 
causes. 

The Air Passages. — In persons who die from asphyxia the mu- 
cous membrane of the larynx, trachea, and bronchi is usually con- 
gested, and the air passages contain a variable quantity of bloody or 
mucous froth. In persons dying in the water from other causes than 
asphyxia these appearances are absent. Foreign substances from the 
■water, such as sand, weeds, etc., or matters regurgitated from the 
stomach, may find their way into the air passages during the act of 
drowning or as a post-mortem occurrence. Thus, in bodies washed 
about on the bottom, sand or mud may get into the air passages for 
a certain distance, from the mechanical action of the water. 



DEATH FROM SUFFOCATION — ASPHXIA. 687 

The Lungs in typical cases are distended so that they fill the 
thorax and cover the heart. The increased size is due partly to con- 
gestion, partly to the presence of the fluid in which the person was 
drowned, which is often inspired during the act of drowning, and 
partly to the distention of the air vesicles with air. While, in cases 
of drowning in which there is a struggle and water is breathed in, 
the lungs contain more or less fluid, this may, as a result of decom- 
position, find its way in greater or less quantity into the pleural cavi- 
ties by transudation, leaving the lungs comparatively empty. It 
should be remembered, however, that a considerable quantity of 
reddish fluid may collect in the pleural cavities under other condi- 
tions than drowning, as a post-mortem change, by transudation from 
the blood vessels and other adjacent tissue. 

The Heart. — In those who die from asphyxia the right cavities 
are usually filled with fluid blood, while the left cavities are empty. 
But where death is due to complex causes this may not be the case. 

The Stomach. — The fluid in which the person was drowned, 
sometimes mixed with sand, weeds, etc., may be swallowed during 
the act of drowning. Sand may wash for a short distance into the 
oesophagus after death, in bodies washing about the bottom. 

The Abdominal Viscera may be congested in persons who die 
from asphyxia. 

In persons dying from syncope, shock, etc., we may find no 
lesions. When the death is partly due to asphyxia and partly to 
■other causes, the conditions will vary in various ways, which need 
not be described in detail here. 

In important cases of doubtful drowning it is desirable to care- 
fully collect and save some of the fluid from the lungs and stomach 
for micro-chemical examination, since the identification of these 
iluids with those in which the person was presumably dro^vned will 
often give certainty to an otherwise doubtful case. 

For the detailed consideration of the anatomical diagnosis of 
drowning, the changes which bodies dead from drowning undergo 
from decomposition, and the factors bearing on the question of sui- 
-cide, homicide, etc., we refer to works on medical jurisprudence.' 

^ IMij, "Legal Medicine," vol. ii., pp. 343-373. Gmj and Fcrricr, "Forensic 
Medicine," pp. 274-285. 



DEATH FROM P01S0]N"I^Q. 



In cases of suspected poisoning which may possibly have a medi- 
co-legal bearing the examination should be made with extreme care 
and thoroughness. The inspection of the body and the examination 
of all the viscera should be thorough and detailed. Every appear- 
ance should be noted at the time and nothing left to the memory. 
It is well to have an assistant record the observations as they are 
made. The disposition of the parts and organs in jars should also 
be noted at the same time. 

It is important to remember that many poisons destroy life with- 
out producing appreciable lesions, and also that many cases of sud- 
den death occur, not due to poisons, and without any discoverable 
cause. 

In bodies which are exhumed for examination the tissues may be 
so changed by decomposition that it is impossible to say whether 
lesions have or have not existed. In such cases the careful and 
separate preservation of the viscera and other parts for chemical ex- 
amination is often all that can be done. For directions for preserving 
tissues and organs for the chemist in medico-legal cases, see Part I. 
(page 37). 

SULPHUEIC ACID. 

The effects of this poison vary with the amount taken and with 
its strength. Death usually takes place in from two to twenty-four 
hours after the taking of the concentrated acid. A case of death 
within an hour is recorded. When the poison is less concentrated 
or its effects less intense, the patient may survive for months. 

The skin of the face about the mouth may be blackened and 
charred by the acid. The mouth and pharynx are of a grayish or 
blackish color, or are covered with a whitish layer, while the deeper 
tissues are reddened. Sometimes these regions escape the action of 
the poison. 

The larynx, trachea, and lungs are sometimes acted on, softened, 
and blackened by the accidental passage of the acid into them.. 



DEATH FROM POISONING. 689 

This may even take place when the acid does not pass into the oeso- 
phagus. 

The oesophagus seldom escapes. It is grayish or blackish col- 
ored, softened, and the mucous membrane comes off in shreds. If 
life is prolonged, cicatrices and strictures are formed. The stomach 
may contain a blackish, pulpy fluid, due to the action of the acid on 
mucus, blood, etc. It is coated on its internal surface with a black, 
sticky layer, beneath which the mucous membrane is reddened. 
The mucous membrane may be blackened in patches or stripes. The 
organ may be contracted and the mucous inembrane corrugated. 
Sometimes perforation takes place and the acid blackens and 
softens the adjoining viscera. In protracted cases cicatrices are 
formed and the organ is contracted. If the poison is dilute there 
may be only the lesions of chronic gastritis. 

The blood is sometimes thickened, syrupy, acid, and may form 
thrombi in the vessels. 

The body may be partially preserved from decomposition, OAving 
to the action of the acid upon the tissues. 

Fatty degeneration of the renal epithelium is mentioned by some 
authors. 

The solution of indigo in sulphuric acid, commonly known as 
sulphate of indigo, produces the same lesions as sulphuric acid, and 
also stains the tissues with which it comes in contact of a dark-blue 
color. It is stated that an indigo-blue tint is often found in the 
mucous membranes after poisoning by pure sulphuric acid.^ 

NITRIC ACID. 

Death may occur very soon after the taking of the poison, but 
does not usually occur for several hours, and may not take pla<"e for 
several days or weeks. 

The surface of the mucous membrane of the mouth, jfj/KYr/y/^r, 
and oesophagus is covered with yellow eschars wherever the acid has 
touched it. Beneath and around the eschars the tissues are con- 
gested and red. The poison may be introduced into the oesophagus 
without acting on the mouth. The sto Dutch contains a viscous, 
sanguinolent, yellow or greenish fluid. The mucous membrane is 
congested, red, swollen and softened, ecchymotic. It is rarely per- 
forated. The duodenum may be inflamed, antl the inflamniation 
extend to its peritoneal coat. The rest of the intestines usually 
escapes the action of the acid. 

The larynx is very frequently acted on by the acid. There are 

^ Woodman and 2Ydf/, "Forensic Medicine and Toxicology,'' ed. 1S77. p. Q3T. 



690 DEATH FROM POISONING. 

yellow eschars, congestion and swelling of the mucous membrane, 
sometimes oedema of the glottis. The trachea may be inflamed and 
the lungs congested. 

If the patient survives the first effects of the poison the lesions of 
chronic inflammation, cicatrization, and contraction may be found 
at a later period. 

The acid nitrate of mercury, if taken in a concentrated form into- 

the stomach, may produce the same lesions as nitric acid. 

« 

HYDEOCHLORIC ACID. 

In fatal cases death occurs on the average in about twenty-four 
hours. The lesions are in general similar to those produced by sul- 
phuric and nitric acids, except that the eschars are usually of a whit- 
ish color at first, becoming, after a time, discolored and disinte- 
grated. It is also more common to find false membranes on the in- 
flamed surfaces. 

OXALIC ACID. 

In fatal cases death may occur within ten minutes (in one case in 
three minutes) or may be delayed for two or three weeks. The pe- 
riod of death does not depend, as do in general the symptoms, upon, 
the amount and concentration of the poison. 

The mucous membrane of the mouth, pharynx, and oesophagus 
is usually white and shrivelled, and easily peeled off, and may be 
covered with brownish vomit from the stomach. The oesophagus, 
may be much contracted. The stomach is usually contracted and 
contains a dark-brown, acid, mucous fluid. The mucous membrane 
of the stomach may be pale, soft, and easily detached, sometimes, 
looking as if it had been boiled in water. Sometimes it is red and 
congested ; sometimes blackened and gangrenous ; sometimes peeled 
off in patches. Perforation is of rare occurrence. If life be pro- 
longed the whitened condition of the mucous membrane is succeeded 
by congestion and inflammation. The small intestines may be in- 
flamed. Inflammation of the pleura and peritoneum, and conges- 
tion of the lungs, are of occasional occurrence. In some cases of 
death from oxalic acid there are no well-marked lesions. 

Potassium oxalate produces the same lesions as oxalic acid. 

TARTARIC ACID. 

This acid is seldom used as a poison, but in large doses may prove 
fatal. The lesions in the cases observed were redness and inflam- 
mation of the mucous membrane of the gastro-intestinal canal. 



DEATH FROM POISONING. 691 



POTASH, SODA, AND THEIR CARBONATES. 

These substances are not commonly used as poisons with suicidal 
or homicidal intent, but may be taken by mistake. They may cause 
death in a few hours, or life may be prolonged for several weeks. 

The mucous membrane of the mouth, pharynx, oesophagus, and 
stomach is softened, swollen, congested, and inflamed, or may be 
peeled off. It may be blackened from local changes in the blood. 
The mucous membrane of the larynx and trachea may also be swol- 
len and inflamed. 

If life is prolonged for some time, cicatrices and strictures of the 
oesophagus and stomach are apt to be produced as a result of the 
reparative inflammation. 

AMMONIA. 

The vapor of strong ammonia may cause death from inflamma- 
tion of the larynx and air passages. The strong solution of am- 
monia produces lesions similar to those of potash and soda. The 
larynx, trachea, and bronchi are frequently inflamed, and may be 
covered with false membranes. Fatal inflammation of the rectum 
and colon has been produced by an enema of strong solution of am- 
monia. 

POTASSIUM NITRATE. 

Accidental poisoning sometimes occurs from large doses of this 
salt. In the observed cases there were intense congestion and in- 
flammation of the stomach and intestines, and in one case a small 
perforation of the stomach. 

For the effects of several infrequently employed salts of the alka- 
lies and alkaline earths, which for the most part produce simple, in- 
flammation of the gastro-intestinal canal, we refer to special works 
on toxicology. 

PHOSPHORUS. 

Poisoning by phosphorus is much more connnon in France and 
Germany than in this country. Some of the forms of rat poison, of 
which this is a frequent ingredient, and the ends of matches, are 
common media for its administration. It is more often used with 
suicidal than homicidal intent. 

The post-mortem appearances vary according to the length of 
time which elapses before death, which may be from a few hours to 
several months. 

If death takes place in a few hours the only lesions may be those 
produced by the direct local action of the poison. The mouth, pha- 



692 DEATH FROM POISONI-NG. 

rynx, and oesophagus usually escape. The stomach may be only 
slightly reddened, or there may be patches of inflammation and 
erosion. The contents of the stomach are often mixed with blood 
and may have the peculiar smell of phosphorus. There may be little 
bits of wood present w^hen the poison has been taken from the heads 
of lucifer matches. It is said that the mucous membrane of the 
stomach may emit a phosphorescent light in the dark. 

If death does not ensue until after several days the lesions are 
more marked. The body is usually jaundiced. There may be ecchy- 
mosis beneath the pericardium, pleura, and peritoneum, in the lungs, 
the kidneys, the bladder, the uterus, the muscles, and the subcuta- 
neous connective tissue, and bloody fluid in the visceral cavities. 

The heart and voluntary muscles, the walls of the blood vessels, 
and the endothelium of the air vesicles of the lungs may be in the 
condition of fatty degeneration. The blood is usually dark and fluid. 

The stomach sometimes presents no very striking changes. There 
may be small circumscribed spots of inflammation, erosion, or gan- 
grene, and occasionally perforation. The most constant change is a 
granular degeneration of the cells which fill the gastric follicles. In 
consequence of this the mucous membrane appears thickened, opaque, 
of white, gray, or yellow color. 

The small intestine appears normal or is congested. 

The liver is found in different degrees of parenchymatous and 
fatty degeneration, and is often stained yellow from the jaundice. 
It is usually increased in size and of a grayish, grayish-yellow, or 
light-yellow color, unless stained' by the bile. Less frequently the 
centres of the acini are congested, or the entire liver is congested, or 
there are small haemorrhages in the liver tissue. The liver may be 
soft, flabby, and smaller than normal. In the interstitial tissue of 
the liver and along the branches of the portal vein there may be 
marked infiltration with small spheroidal cells. 

The kidneys often present parenchymatous and fatty degenera- 
tion of the epithelium. The niesente7nc lymph nodes may be soft 

and swollen. 

ARSENIC. 

This poison is very frequentl}^ employed with suicidal intent. 
Death may occur in a longer or shorter time from the direct irrita- 
tive effects of the poison upon the gastro-intestinal canal, with the 
symptoms which usually accompany the ingestion of irritant poisons ; 
or it may occur with symptoms of collapse, or coma, or shock ; or 
the symptoms may resemble those of cholera. The average time of 
death in acute fatal cases is about twenty hours, but death has 
occurred in twenty minutes and has been prolonged for two or three 
weeks. 



DEATH FROM POISONING. 693 

The mouth, pharynx, and oesophagus may be inflamed, but are 
more frequently unaltered. The stomach may be empty or contain 
mucus mixed with blood. The arsenic, in substance, may be found 
adherent to the mucous membrane or mixed with the contents of the 
organ. It has, in rare cases, been found encysted in the stomach in 
considerable quantity. When invisible to the naked eye a micro- 
scopical examination of the stomach contents will not infrequently 
reveal characteristic crystals of arsenious acid or some of its com- 
pounds. The stomach may be contracted and its mucous membrane 
€orru gated. The entire inner surface may be red and inflamed, or 
there may be patches or streaks of inflammation or deep congestion. 
The inflamed and congested patches may be thickened and covered 
with false membrane mixed with larger and smaller particles or 
masses of the poison. Ulceration, perforation, and gangrene are 
rare. Blood may be extravasated into the mucosa and submucosa, 
and with the congestion give the mucous membrane a very dark-red 
or brown appearance. Frequently the mucous membrane is studded 
with small petechise. Sometimes the arsenic is converted in the 
stomach into the yellow sulphide. There may be acute gastritis, 
even when the poison is absorbed by the skin or otherwise and not 
introduced into the stomach. Taylor mentions a case in which the 
coats of the stomach were thickened and gelatinous, but not con- 
gested. The epithelium of the gastric glands may undergo granular 
and fatty degeneration. 

The entire length of the intestine may be congested and inflamed, 
but the action of the poison does not usually extend beyond the duo- 
denum. In some cases the solitary lymph nodules, Peyers 
patches, and the mesenteric nodes are swollen. Inflammation of 
the Madder and peritoneum, and congestion and oedema of the 
brain, have been observed, but are neither frequent nor in any Avay 
characteristic. 

Fatty degeneration of the muscles, liver, kidneys, blood vessels, 
and vesicular epithelium of the lungs may be produced in arsenical 
poisoning. 

Alterations in the spinal cord indicative of acute myelitis have 
been described by Popon ^ as occurring in dogs poisoned with arse- 
nious acid. 

The walls of the stomach and intestines and other parts of the 
body may be preserved from decomposition for a long time after 
death by arsenical poisoning. 

It should always be borne in mind, in examining cases of sus- 

^ _ 

^ Popon, " Ueberdie Venimlerungen im Riickeninarke nach Vergiftuiiij init Arseu, " 
etc., Vii'cli. Arch., Bd. xciii., j). i^ol. 



694 DEATH FROM POISONING. 

pected arsenical poisoning, that death may be produced by arsenic 
and its compounds without any appreciable lesions. While in gene-^ 
ral it may be said that in the cases in which no lesions are discovered 
death has been rapid, the death may be delayed in such cases until 
long after a period at which, in other cases, marked inflammatory 
changes have occurred. 

Compounds of arsenic, such as the chloride and sulphide, and the 
arsenite (Scheele^s green, Paris green), are sometimes used for sui- 
cidal purposes, and produce lesions similar to those of arsenious 
acid. Paris green is a favorite article in New York, particularly 
among Germans, for suicidal purposes. It is usually taken in con- 
siderable quantities, and is often found in the stomach after death. ^ 

COEROSIVE SUBLIMATE. 

The mucous membrane of the mouth and throat may be swollen, 
inflamed, or have a grayish-white appearance. The oesophagus may 
be swollen and white, or congested, or unaltered. The mucous mem- 
brane of the stomach is usually congested or inflamed, or there may 
be patches of softening, ulceration, or gangrene. Perforation is of 
rare occurrence. Small ecchymoses in the mucosa are not uncom- 
mon. Sometimes there is little or no change in the stomach. Some- 
times the mucous membrane of the stomach is slate-colored from the 
deposition of metallic mercury from the decomposed salt. The in- 
testines may appear normal, or there may be patches of congestion 
and ecchymosis. 

The larynx and trachea may be congested. The kidneys may^ 
show parenchymatous and fatty degeneration of the epithelium. 

LEAD. 

The 'different preparations of lead may prove fatal either from 
the immediate effect of large doses or from the gradual effects of re- 



^ It is advisable, in cases of suspected arsenic poisoning, particularly if the body 
have lain for some time, as in exhumations, to preserve not only all of the internal 
organs entire for the chemist, but also portions of the muscles (back, thigh, arm, and 
abdomen), and also one of the long bones, preferably the femur, since arsenious acid 
and its compounds are quite diffusible, and may be present in proportionately larger 
quantity in other parts than in the gastro-intestinal canal. It is desirable to save the 
whole of the internal organs, and to weigh the muscle and bones as well as the whole 
body at the autopsy, in order that the calculations of the chemist, in case arsenic be 
found, may rest upon a definite basis, and be as little as possible dependent upon esti- 
mates, whose value may be questioned by lawyers should the case come into the 
courts. 



DEATH FROM POISONING. 695- 

peated small doses. Although there may he marked symptoms dur- 
ing life, the post-mortem lesions are few and variahle. 

Large doses may produce acute gastritis, and sometimes a whiten- 
ing of the mucous membrane. The intestines art; generally con- 
tracted, and there may be fatty degeneration of the renal epithelium ;. 
very frequently there are no appreciable lesions. 

In chronic lead poisoning the intestines may be contracted, the 
voluntary muscles flabby and light-colored, or partially replaced by 
connective tissue, and there may be chronic meningitis. 

COPPER. 

Acute poisoning by salts of copper is not very common, but it is 
of occasional accidental occurrence, and the salts are infrequently 
used with suicidal intent. The sulphate and acetate are the most 
important salts in this respect. Soluble salts of copper may be 
formed in the use of copper cooking utensils, and accidents most fre- 
quently occur in this way. 

The post-mortem appearances are somewhat variable. The 
pharynx and oesophagus may be somewhat inflamed or unchanged. 
The mucous membrane of the stomach and intestines may be in- 
flamed, ulcerated, or gangrenous, and perforation and peritonitis 
may occur. The mucous membrane may have a diffuse greenisk 
color, or particles of the salt may be found adhering to it. 

TARTAR EMETIC. 

This preparation of antimony may prove fatal when administered 
in a single large dose or in repeated small doses. The post-n-«.orteni 
lesions are not constant. In cases of chronic poisoning there are 
usually no appreciable lesions. 

In cases of acute poisoning there may be evidence of acute in- 
flammation of the oesophagus, stomach, intestines, and perito- 
neum. Sometimes the stomach exhibits no lesions, while the intes- 
tine is involved. The larynx and lungs may be deeply congested. 



VEGETABLE IRRITANTS. 

Aloes, colocynth, gamboge, Jalap, scammony, sarin, crofon 
oil, colchicum, veratria, hellebore, elateriuDf, and turpentine. 

All these drugs may produce poisonous effects. The post-mortem 
lesions are congestion, inflammation, and sometimes ulceration of 
the gastro-intestiual mucous membrane ; but these lesions are some- 
times present and sometimes absent. 



696 DEATH FROM POISONING. 



CANTHAEIDES. 

This substance may be given in powder or tincture. The entire 
length or only a portion of the alimentary canal may be congested 
or inflamed. There may be patches of gangrene of the mucous 
membrane of the stomach. When the poison was taken in sub- 
stance a microscopical examination of the contents of the alimentary 
canal or of the mucous membrane may reveal the glistening green 
and gold particles of the fly. 

The kidneys, ureters, and bladder may be congested and in- 
flamed. There is sometimes congestion of the brain and its mem- 
branes. 

OPIUM. 

The post-mortem appearances in persons who have died from 
opium poisoning are inconstant and not characteristic. Congestion 
of the brain and its membranes, with serous effusion in the mem- 
branes and ventricles, and congestion of the lungs, are changes oc- 
casionally seen, but they are frequently entirely absent, and when 
present are not characteristic of death from this poison. 

POISONOUS FUNGI. 

The action of these substances varies greatly, and the post-mor- 
tem appearances are inconstant and not characteristic. In general, 
when any lesions are present, they are those of gastro-intestinal irri- 
tation or of venous congestion, or both. 

Microscopical examination may reveal characteristic fragments of 
fungi in the contents of the aHmentary canal. 

HYDROCYANIC ACID. 

This poison in fatal doses may destroy life in a very short time. 
'The post-mortem appearances are inconstant and not characteristic. 
The skin may be Hvid and the muscles contracted. The stomach 
may be congested or normal. The most frequent internal appear- 
ances are those of general venous congestion. Under favorable con- 
ditions the odor of prussic acid may be detected in the stomach or 
blood or brain, or other parts of the body. It may be absent in the 
stomach and present in other parts of the body. If the patient have 
lived for some time the odor maj' be absent altogether. 

Cyanide of potassium may produce the same lesions as prussic 
:acid, and there is the same inconstancy in their occurrence. 

Nitrobenzole, — This substance produces general venous conges- 



DEATH FROM POISONING. 



697 



tion, and the odor of the oil of bitter almonds may be more or less well 
marked in the body after death. 

CARBOLIC ACID. 

When this poison is taken into the stomach the mucous mem- 
brane of the mouth, oesophagus, and stomach may be white, cor- 
rugated, and partially detached in patches, and the edges of the 
affected parts may be hyperaemic or there may be patches of extra- 
vasation. Brownish, shrunken patches may be present about the 
mouth. The brain and meninges may be congested. There may 
be congestion and oedema of the lungs, and congestion of the liver 
and spleen. The blood is usually dark and fluid. The urine is. 
usually of a dark or greenish color. The odor of the poison may be 
evident in the body and in the urine. 

ALCOHOL. 

The different preparations of alcohol, when taken in concentrated 
form or in large quantities, sometimes produce sudden coma and 
death in from half an hour to several hours. In acute poisoning, if 
death have followed soon after the ingestion of the poison, the body 
may resist decomposition for an unusual length of time. The stomach 
and tissues may even have a more or less well-marked alcoholic odor. 
The stomach, and even the oesophagus and duodenum, may be of a 
deei>red color. There may be punctiform ecchymoses in the gastric 
mucous membrane. In many cases the stomach is apparently quite 
normal. There is apt to be venous congestion in some of the internal 
organs, but this is not constant. There is frequently congestion and 
sometimes extravasation of blood in i\\Q brain Sin^ii^ membranes, 
and oedema of the membranes or of the brain substance, or both. 
There may be a serous effusion in the ventricles of the brain. The 
bladder is frequently distended with urine, as in other cases in which 
death is preceded by a period of unconsciousness. 

Chronic alcohol poisoning is of a different nature. The subjects 
of it may die from some other disease, or they die after a debauch 
without anything else to account for their death. In the latter case 
there may be delirium tremens, or the patient dies exhausted and 
comatose. Chronic alcoholism is not infrequently mistaken clinically 
for meningitis. The post-mortem lesions are sometimes marked, 
sometimes absent. There may be chronic pachymeningitis, resulting* 
in thickening of the dura mater and its close adherence to the skull. 
HlnQ pia mater may be thickened and oedematous. The 6/-(//// may 
be normal or oedematous or atrophied. The lungs are frequentlj' 



'698 DEATH FROM POISONING. 

congested. The heart may be thickly covered with fat, and its walls 
may be flabby and fatty. The stomach frequently presents the 
lesions of chronic gastritis. The liver may be cirrhotic, with or with- 
out fatty infiltration. The kidneys may present the lesions of paren- 
chymatous or fatty degeneration or of chronic diffuse nephritis. 

It should always be remembered, however, that all or a part of 
the above lesions may be absent in the bodies of drunkards, and, 
furthermore, that the same lesions may be due to other causes. 

CHLOROFORM. 

Chloroform may cause death when it is taken in fluid form into 
the stomach or when inhaled. Death from swallowing liquid chlo- 
Toform is rare, and its immediate cause is usually uncertain. The 
post-mortem changes are variable ; sometimes there are no lesions. 
In some cases there is simple reddening of the gastric mucous mem- 
brane ; occasionally there is acute gastritis or ulceration of the mu- 
cous membrane. The odor of chloroform may or may not be evi- 
dent. Discoloration and softening of the mucous membrane of the 
pharynx, oesophagus, and duodenum have been observed. There 
may be general venous congestion ; the heart may be flabby. Bub- 
bles of gas have been frequently seen in the blood, but this is not 
characteristic. Death from inhalation of chloroform is a not infre- 
quent accident in surgical practice. After death from inhalation 
the results of the examination are usually quite negative. 

ETHER. 

The inhalation of ether occasionally causes death. The post- 
mortem examination is negative. The ingestion of fluid ether may 
induce inflammation of the stomach. The odor of ether may be per- 
ceptible if the autopsy is made soon after death. 

CHLORAL HYDRATE. 

There are no characteristic post-mortem appearances after death 
by chloral. Hypersemia of the brain, and the odor of the drug, have 
been noticed. 

STRYCHNIA— NUX VOMICA. 

The post-mortem appearances after poisoning by these drugs are 
not characteristic and are inconstant. The body is usually relaxed 
at the time of death, but the rigor mortis usually comes on early and 
remains long. There may be congestion of the brain and spinal 
.cord, and sometimes of the lungs and stomach. 



DEATH FROM POISONING. 699 

CONIUM, ACONITE, BELLADONNA, LOBELIA INFLATA, 
DIGITALIS, STRAMONIUM. 

These vegetable poisons are administered in their natural form of 
leaves, berries, and roots, or in tinctures, infusions, and extracts, or 
in the form of their active alkaloid principles. 

If the leaves, berries, or seeds are given they may be detected in 
the contents of the stomach by microscopical examination. Other- 
wise the results of autopsies are not characteristic. 

The brain and its membranes, and the lungs, may be congested. 
The stomach may present patches of congestion, inflammation, and 
extravasation, or its entire mucous coat may be inflamed, or it may 
appear normal. 

Microscopical examination of the contents of the alimentary canal 
may reveal characteristic seeds or fragments of leaves.' 

CARBONIC OXIDE. 

This is one of the gases formed in the burning of charcoal, and 
forms one of the ingredients of illuminating gas. The most charac- 
teristic post-mortem appearance is the cherry-red color of the blood, 
and of the tissues and viscera which contain blood. The presence of 
carbonic acid in the gas may obscure the bright red of the carbonic 
oxide by the dark color which it induces in the blood. 

CARBONIC ACID. 

The lesions are essentially those of asphyxia, but the brain is said 
to be more frequently congested than in asphyxia by simple obstruc- 
tion of respiration. 

For a more detailed consideration of poisons, their effects, modes of detection, 
etc., consult Ta^^o?' on Poisons ; J!fctscM<x's " Handbucli der gericiitlichen Medicin," 
Bd. ii,; Woodman and Tidy, "Forensic Medicine." Wormlcy's " Micro-cliemistiy of 
Poisons" contains a series of good plates of the microscopical appearance of various 
forms of crystals of poisonous substances. 

Lesser's " Atlas der gericiitlichen Medicin " contains a series of fine colored plates 
showing the appearance of the stomach after the action of various poisons. The 
smaW work of Ouy and Ferrier on "Forensic Medicine" contains in very compact 
and reliable form much information on the general subjects treated in the foregoing 
section. 

^ Consult Oai/ and Ferrier, "■ Forensic Medicine," p. 534. 



INDEX. 



Abbe's condenser, use of, in examining 

bacteria, 183 
Abdominal cavity, examination of, in 
adults, 27 
cavity, examination of, in 

children, 44 
cavity, methods of opening, 

18 
cavity, serum in, as a result 
of post-mortem changes, 19 
organs, post-mortem changes 

in, 19 
pregnancy, 614 
Abscesses, formation of, in inflammation, 

92 
Acarus scabiei, 116 
Achorion Schonleinii, 146 
Acid, carbolic, poisoning, lesions of, 697 
carbonic, poisoning, lesions of, 699 
chromic, use of, in decalcifying 

tissues, 47 
hydrochloric, poisoning, lesions 

of, 690 
hydrocyanic, poisoning, lesions of, 

696 
nitric, poisoning, lesions of, 689 
nitric, use of, in decalcifying tis- 
sues, 47 
osmic, use of, in preserving tissues, 

48 
oxalic, poisoning, lesions of, 690 
picric, use of, in decalcifying, 47 
sulphuric, poisoning, lesions of, 

688 
tartaric, poisoning, lesions of, 690 
Aconite poisoning, lesions of, 699 
Acrania, 315 
Actinomyces, 206 
Addison's disease, lesions of, 674 
Adenoma, general consideration of, 263 
Adrenals, 29, 541 

Agar, use of, in cultivating bacteria, 136 
Ague cake, 523 
Aguillula, 116 

Air, presence of, in blood, air emboli, 70 
Alcohol poisoning, lesions of, 697 

use of, in preserving tissues, 48 
Alimentary canal, 441 
Aloes poisoning, lesions of, 695 
Alveolar sarcoma, 248 

60 



Ammonia poisoning, lesions of, 691 
Amcfiba coli, occurrence of, in dvsentery, 

103 
Amyelia, 330 
Amyloid degeneration, 80 

degeneration, methods of stain- 
ing tissues in, 81 
Anaemia, changes of blood in, 64, 65 

changes of marrow cells in, 651 
effects of, on tissues and organs, 

57 
pernicious, 673 
Anencephalia, 315 
Aneurism, cirsoid. 419 

dissecting, 420 
false, 423 

miliary, of brain, 304 
of the aorta, 421 
of the blood vessels, 421 
of the coronary arteries, 421 
of the heart, 411 
of the heart valves, 410 
of the pulmonary arteries, 421 
spurious, 423 
varicose, 424 
Aneurismal varix, 424 
Angina, bacteria in, 161 
Angiomata, general characters of, '4.58 
Angio-sarcoma, 247 
An!iydra3mia, 6-^ 

Anilin colors, uses of, in staining bac- 
teria, 132 
Anilin-gentian-violet solution, formula 

for, 132 
Ankylostomum duodenale, 477 
Anthrax, 167 

bacilli, 168 
Anus, atresia of, 464 
Aorta, examination of arch of, before re- 
moval from body, 22 
aneurism of. 421 
atheroma of, 419 
malformations of. 395 
stenosis of. 422 
Ai)oplectic clots, methods of examining, 

Apoplexy of brain, 304 

placental, 615 
Appendix vormiforniis. 474 
Arachnoid, nature of, 284 



702 



INDEX. 



Archiblast, 232 

Arsenic poisoning, lesions of, 692 

Arteries, aneurism of, 419 

atheroma of, 419 

dilatation of, 419 

inflammation of (see Arteritis), 
414 

rupture of, 423 

stenosis of, 422 

sclerosis of, 417 

terminal, 61 

tumors of, 424 

wounds of, 433 
Arterio-sclerosis, 414 
Arteritis, acute, 414 

chronic, 414 

tubercular, 419 
Arthritis, 656 
Arthropods. 116 
Ascaris lumbricoides, 111, 477 
maritima, 111 
mystax, 111 
Ascites, tubercular, 485 
Asiatic cholera, 209 
Aspergillus, 145 
Asphyxia, 683 
Ataxia, locomotor, 327 
Atelectasis, 358 
Atheroma, 419 
Atrophia musculorum lipomatosa, 667 

Bacilli, chain forms of, 142 
color-forming, 143 
curved forms of, 142 
mobility of, 142 
pathogenic, 143 
saprophytic, 143 
Bacillus, 142 

acidi lactici, 143 

anthracis, 167 

cholerse Asiaticse, 210 

coli communis, 143, 152, 205 

diphtherige, 198, 200 

leprae, 183 

mallei, 188 

of malignant oedema, 204 

pneumoniae, 204 

prodigiosus, 143 

pyocyanus, 148, 152 

pyogenes foetidus, 152 

pyogenes soli, 152 

rhinoscleromatis, 186 

tetaui, 201 

tuberculosis, 175 

tuberculosis, relation of, to sup- 
puration, 152 

typhosus, J, 95. 197 

typhosus, relation of, to sup- 
puration, 152 
Bacteria, 119 

action of disinfectants on, 121 

aerobic, 122 

agar as culture medium for, 136 

artificial cultivation of, 134 

as a cause of tumors, 229 



Bacteria, beef tea as culture medium for, 
136 
bibliography of, 139 
Browuian movement in, 141 
capsule of, 120 
chemotaxis in, 121, 122 
cilia of, 122 
classification of, 139 
cultivation of, 134 
filiform, 142 

gelatin nutrient as culture me- 
dium for, 135 
Grams method for staining, 132 
influence of disinfectants on, 

121 
influence of temperature on, 121 
methods of studying, 130 
milk as culture fluid for, 136 
mode of collecting specimens to 

be examined for, 1 39 
morphology and physiology of, 

119-122 
parasitic, 140 
pathogenic. 143, 144 
plate cultures of, 136 
potatoes as culture medium for, 

135 
protein of, 125 
putrefaction dependent upon, 

122 
pyogenic, 149 

relations of, to disease, 123, 127 
• rod-shaped, 142 
saprophytic, 143, 144 
spheroidal, 140, 141 
spiral-shaped, 144 
spores of, 120 
staining, 130, 131 
zoogloea colonies of, 120 
Bacterial diseases, hereditary predisposi- 
tion to, 95 
diseases, conditions influencing 

occurrence of, 127 
diseases, immunity in, 128 
origin of disease, proofs of, 94 
toxins, 123 
Balanitis, 6. '4 
Balantidium coli, 105 
Beef tea as culture medium for bacteria, 

136 
Belladonna poisoning, lesions of, 699 
Bile duct, examination of, at autopsies, 

32 
Biliary passages, lesions of, 514 
passages, calculi of, 516 
passages, tumors of. 518 
Bladder, gall, bacteria in, 569 
gall, lesions of, 514 
urinary, calculi in, 569 
urinary, in children, 45 
urinary, cysts of, 568 
urinary, dilatation of, 564 
urinary, diverticula of. 564 
urinary, examination of. 34. 35 
urinary, foreign bodies in, 569 



INDEX. 



703 



Bladder, urinary, hsemorrhage of, 566 
urinary, heruiye of. 565 
urinary, hypersemia of, 565 
urinary, hypertrophy of, 565 
urinary, inflammation of, 566 
urinary, malformations of, 563 
urinary, parasites of, 568 
urinary, perforation of, 565 
urinary, removal of, 34, 35 
urinary, rupture of, 565 
urinary, tumors of, 568 
Blood, changes in circulation of, 57 
changes in composition of, 63 
coagulability of, 59, 63 
diseases characterized by altera- 
tions in composition of, 673 
distribution of, in life and death, 9 
extravasated, changes in, 58 
examination, 67 
foreign bodies in, 69 
parasites in, 70 
Blood vessels, atrophy of, 412 

calcification of, 413 
degeneration, amyloid, 413 
degeneration, fatty, 413 
degeneration, hyaiin, 413 
formation of, in granula- 
tion tissue, 95 
hypertrophy, 413 
inflammation of, 414 
Bone, abscess, 642 
atrophy, 652 
caries, 647 
cysts of, 655 
decalcifying, 47 
dislocations of, 635 
fractures of, 635 
h.Tmorrhage, 635 
hypersemia, 635 

inflammation of (see Osteitis), 638 
leuksemic, 651 
necrosis, 646 
osteomalacia, 650 
osteomyelitis, 644 
parasites of, 655 
rachitic changes in, 647 
sequestrum of, 646 
syphilitic, congenital, 643 
tubercular, 490 
tumors of, 652 
wounds of, 635 
Bothriocephalus cordatus, 111 
cristatus, 111 
latus, 110, 478 
Brain, abscess, 309 
anojmia, 303 

aneurism of, miliary, 304 
atrophy of, 306 

axis, mode of separation of, 15 
cysts of, 308 
degeneration of, 301 
degeneration of, secondary, 306 
embolism, 300 

examination of, at autopsies, 11 
hajmorrhage, 303 



Brain, hernia, 195 

holes in, 308 

hyperiemia of, 303 

hypertrophy of, 306 

inflammation (see Encephalitis), 
308 

inflammation, syphilitic, 311 

inflammation, tubercular, 312 

lesions of, in general paresis of in- 
sane. 313 

membranes, lesions of, 279 

malformations of, 315 

mantle, mode of separation of, 15 

oedema, 303 

parasites, 315 

pigmentation, 313 

preservation and hardening of, 
16 

sand, 249, 282 

sclerosis of, 310 

softening of, 301 

thrombosis, 300 

tubercles of, solitary, 312 

tumors of, 314 

ventricles of, 295 

weight of, 11 

wounds of, 307 
Bright's disease, 544 

Bronchi, inflammation of (see Bronchitis), 
349 
preservation of, 25 
tumors, 353 
Bronchiectasia, 352 , 

Bronchitis, 364 
Broncho -pneumonia, 364 
Bronze liver, 498 

Brood capsules of echinococcus, 109 
Brownian movement in bacteria, 141 
Bubo, 432 
Burning, death from, 681 

Cacao butter for embedding, 50 
Cachexia, development of, with malig- 
nant tumors, 118 
strumipriva, 540 
Cadaveric discolorations, 4 
Ccecum, inflammation of, 474 
Calcareous degeneration, 85 
Calcification. b5 
Calculi, biliar}'-, 516 

pancreatic, 533 

prostatic. 634 

renal, 561 

vesical, 569 
Callus, 99, 100 
Calvarium, examination of, at autopsies, 

10 
Cancer (see Carcinoma), 265 
Cantharides poisoning, lesions of, 696 
Capillaries, blood, lesions of, 428 
Capsule in bacteria. 120 

suprarenal, examination of, at 
autopsies, 29 

suprarenal, lesions of, 541 
Caput succedaneum, 41 



704 



INDEX. 



Carbolic acid poisoning, lesions of, 697 
Carbonic acid poisoning, 699 

oxide poisoning, 699 
Carbuncle, 167 
Carcinoma, 265 

colloid, 27-t 
cylindrical-celled, 273 
durum. 273 
tibro-, 273 
flat celled, 269 
forms of. 269 
gland- celled. 273 
medullary, 274 
melanodes, 276 
molle, 274 
myxomatodes, 275 
telangiectoides, 274 
Caries of bone, 647 
Carnoy's solution for fresh tissues, 46 
Casts, preservation of, 50 
Cell division. 72 
Celloidin for embedding, 50 
Cephalhaematoma, 42 
Cephalocele, 316 
Cercomonas intestinalis, 105 
Cestoda, 106 
Chancre. 185 
Charbou, 167 
Charcot's crystals, 651 
Cheeks, lesions of, 44 1 
Cheesy degeneration, 77 
Chemotaxis, 122, 126 
Children, new-born, autopsies on, 38 

new-born, changes in, imme- 
diately following birth, 40 
new born, internal examination 
of, 41 
Chloral hydrate poisoning, lesions of, 698 
hydrate, preserving action on 
tissues. 53 
Chloroform poisoning, lesions of, 698 

preserving action on tissues, 
53 
Chloroma, 249 
Chlorosis, 673 
Cholera Asiatica, bacteria of, 209 

Asiatica. lesions of, 209 
Cholesteatoma, 250 

Cholesterin crystals in brain softening, 
301 
crystals in fatty degenera- 
tion, 79 
Chondroma, 251 
Choroid plexus, lesions of, 295 
Chromic acid for decalcifying, 47 

acid mixture for hardening tis- 
sues, 50. 53 
Cicatricial tissue. 97 
Cirrhosis of the liver. 503 
Cirsoid aneurism, 419 
Clitoris, malformations of, 574 
Cloacae in intestine, 463 
Clots, apoplectic, in brain, 304 

heart, 411 
Cloudy swelling, 78. 87 



Coagulation necrosis, 76 

Cocci, 140, 141, 142 

Coccidium oviforme, 104 

Cohnheirri's theory of embryonal origin 

of tumors, *^29 
Colchicum poisoning, lesions of, 695 
Colitis, amoebic, 473 

catarrhal, acute, 468 
catarrhal, chronic, 474 
croupous, 471 
follicular, 472 
nodular, 472 
Colloid carcinoma, 274 

degeneration, 83 
Colocynth poisoning, lesions of, 695 
Colon bacillus, 205 
Comma bacillus, 210 
Condylomata, syphilitic, of penis, 624 
syphilitic, of vulva, 576. 
Conium poisoning, lesions of, 699 
Consumption, 379 
Contagious diseases, 148 
Contagium, 148 
Contusions, ante-mortem and post-mor- 

tem, 7 
Cooling of the body, post-mortem, 6 
Copper poisoning, lesions of, 695 
Cord, spinal, 317 
Corpora aliena articulorum, 660 

amylacea, 81, 299 
Corrosive sublimate poisoning, lesions of,. 

694 
as hardening agent, 
49 
Cowper's glands, 634 
Craniotabes, 649 

Croton oil poisoning, lesions of, 695 
Croupous inflammation, 160 
Cryptorchismus, 626 
Cryptogenetic pyaemia, 158 
Cutis anserina, 686 
Cyanide of potassium poisoning, lesions. 

of, 696 
Cyclopia, 315 
Cylindroma, 248, 264 
Cysticercus cellulosse, 106, 107, 477 

taeniae mediocanellatae, 108 
Cystin calculi, 570 
Cystitis, catarrhal, 566 
croupous, 567 
tubercular, 567 
gangrenous, 56T 
Cystocele, 565, 577 
Cysto-sarcoma, 249 
Cysts, classification of, 233 
cerebellar, 314 
echinococcus, 109 
multilocular. of ovary, 605 
of ovary, 610 
of parovarium, 611 
preservation of, for museums, 5S 
Czenzynski's solution, 68 

Death, causes of. 3 
Decalcification of bone, 47 



INDEX. 



705 



Decomposition, post-mortem, 5 
Degeneration, acute, 77, 87 
amyloid, 80 
calcareous, 85 
cheesy, 77 
colloid, 83 
fatty, 78 
glycogen, 82 
granular, 77, 87 
liyalin, 84 
lardaceous, 80 
mucous, 82 

parenchymatous, 77, 87 
waxy, 80 
Degenerations, secondary, in the nervous 

system, 306, 320 
Delafield's osmic acid mixture, 49 
Dermoid cysts, 234, 610 
Diabetes, 679 

Diapedesis, haemorrhage by, 58 
in inflammation, 90 
Digitalis poisoning, lesions of, 699 
Diphtheria, 198 

pneumonia in, 370 
pyogenic cocci in, 200 
Diphtheritic bacillus, pseudo , 200 
Diplococcus lanceolatus, 162 

intracellularis meninsritidis. 

156 
pneumoniae of Friinkel, 162, 

359 
relations of, to suppuration, 
152 
Disinfectants, action of, on bacteria, 121 
Distoma haematobium, 106 
hepaticum, 106 
lanceolatum, 106 
sinense, 106 
Dochmius duodenalis, 113 
Drowning, lesions of, 685 
Drysdale's corpuscles, 607 
Duodenum, examination of, 31 

ulcers of, 468 
Dura mater, examination post-mortem 
of, 10 
mater, haemorrhage of, 279 
mater, inflammation of, 280 
mater, thrombosis of longitudinal 

sinuses of, 280 
mater, tumors of, 283 
mater spinalis, inflammation of 

(see Pachymeningitis), 317 
mater spinalis, parasites of, 318 
mater spinalis, tumors of, 318 
Dyscrasia of tumors, 227 
Dysentery, 468, 473 
Dysmenorrhciea membrauacca, 586 

Ecchondroses, 252 

Ecchymoses of skin, post-mortem, 7 

nature of, 5d 
Echinococcus, 108 

cysts, i>reservati()u of, fm- 

museums, 53 
exogena, 110 



Echinococcus, multilocularis, 110, 513 

scolecipariens, 110 
EhrUch's solution for blood staining, 69 
Elaterium poisoning, lesions of, 695 
Electricity, death from, 682 
Elephantiasis, 430 

of vulva, 576 
Embedding, 50 
Emboli, fat, 70 

infectious, 62 
Embolic infarctions, most frequent seat 

of, 62 
Embolism, effects and occurrence of, 61 
Embryonal layers, 231 

origin of tumors, Cohnheim's 
hypothesis of. 229 
Emigration of white blood cells, 89 
Emphysema of lungs, 356 
Empyema, pneumococci in, 162 
Encephalitis, 308 

in new-born, 311 
Encephalocele, 316 
Encephaloid cancer, 274 
Endarteritis, 414 

Endartery (see Terminal artery), 61 
Endocarditis, acute, 405 

bacteritic, 406 
chronic. 408 
malignant, 406 
mycotic, 406 
tubercular, 409 
ulcerative, 409 
Endocardium, structure of, 404 

discolorations of , 2-1 
fatty degeneration of, 402 
inflammation of, 404 
Endometritis, acute catarrhal, 585 

chronic catarrhal, 588 
croupous, 588 
puerperal, 589 
syphilitic. 589 
tubercular, 588 
Endophlebitis, 426 
Endothelioma, general characters and 

situation of, 249 
Endothelium of peritoneum, etc.. em- 
bryonal origin of, 266 
vascular changes in, in 
syphilis. 184 
Enostoses, 653 

Enteritis, catarrhal, acute. A^^^^ 
catarrhal, chronic, 467 
croupous, 467 
suppurative, 467 
Eosin, use of, in staining- tissues, 5J 
Eosinophile leucocytes. 65 
Ependyma, cysts of. 299 

inllatnmntions of ^soe Ei>ea- 

dymitis). 296 
]iarasitos of. 299 
tubercles of, 293 
tunuM's of. 298 
Ependvmitis. 296 
Epiblast. 232 
Epididymitis, acute. 628 



706 



INDEX. 



Epispadias, 623 

Epithelial pearls in epithelioma, 270 

tumors, 265 
Epitheliomata, 269, 273 
Epulis, 246 
Erysipelas, 153 

Ether poisoning, lesions of, 698 
Exostoses, 253. 653 
Extra- uterine pregnancy, 613 
Exudations, 59 

mode of preserving, 50 
Exudative inflammation, 88, 92 

Fallopian tubes, changes in size and po- 
sition of, 611 
tubes, cysts of, 613 
tubes, dilatation of, 612 
tubes, hsemorrhage of, 6l2 
tubes, inflammation of (see Sal- 
pingitis), 612 
tubes, malformations of, 611 
tubes, tumors of, 613 
False membrane in croupous inflamma- 
tion, 91 
Famine fever, 213 
Farcy, 187 
Fat, 69 

in blood, 69 

necrosis in pancreas, 533 
pericardial, atrophy of, 403 
Fatty degeneration, 78 

infiltration, 78 
Favus, 146 

Female generative organs, lesions of, 574 
Fever, inflammatory (see Pyaemia), 157 
malarial, lesions and micro-organ- 
isms of, 221 
relapsing, 213 
scarlet, 216 
splenic, lesions and bacteria of, 

167 
suppurative (see Pygemia), 157 
surgical (see Pyaemia), 157 
traumatic (see Pvoemia), 157 
typhoid, 189 ' 
typhus, 218 
yellow, 220 
Fibrin, formation of, in inflammation, 

88, 90 . 
Fibroblasts, 96 

Fibro carcinoma (scirrhous), 274 
Fibro lipoma, 251 
Fibro myxoma, 240 
Fibro-sarcoma, 243 
Fibroma, 237 

intracanalicular, 239 
Filaria medinensis, 1 1 5 

sanguinis hominis, 1 15 
Flemming's osmic acid mixture, 48 

chromic acid mixture, 53 
Flukes, 106 

Fcetal tissues, preservation of, 45 
Fa?tus, examination of, 38 
Fractures, ante-mortem and post-mor- 
tem, 8 



Fractures, healing of, 98 

Frankel, pneumococcus of, 162 

Freezing microtomes, 46 

Fresh tissues, method of studying, 54 

Fuchsin as stain for bacteria, 130 

Fungi, 119 

Fangus poisoning, lesions of, 696 

Gall bladder, calculi of, 516 

dilatation of, 516 
inflammation of, 514 
tumors of, 518 
Gall ducts, calculi of, 516 

constriction and occlusion of,, 

516 
dilatation of, 516 
inflammation of, 514 
tumors of, 518 
Gamboge poisoning, lesions of, 695 
Gangrene of the lung,. 358 

of the mouth, 443 
Gastritis, catarrhal, acute, 454 
catarrhal, chronic, 455 
croupous, 455 
phlegmonous, 456 
suppurative, 456 
toxic, 457 
Gelatin, culture medium for bacteria, 135 
Generative organs, female, lesions of, 574 
organs, male, lesions of, 622 
Gentian-violet stain for bacteria, 130, 132' 
Giant cells, 171, 174 
Giant- celled sarcoma, 245 
Glanders, 187 
Glioma, 254 
Glio-sarcoma, 245 
Glossitis, 445 
Glottis, oedema of, 339 
Gluge's corpuscles, 302, 323 
Glycogen degeneration, 82 
Goitre, 537 
Gonococcus, 165, 572 
Gonorrhoea, 165, 572 
Gout, 678 

Gram's method of staining bacteria, 132 
Granular degeneration, 77 
Granulation tissue, 95, 96 
Granulomata, infectious, 235 
Gray degeneration, secondary, in spinal 

cord, 320 
Grippe, 202 
Guinea- worm. 115 
Gummata, 184, 185 

Haemangioma, 259 
Haematocele, 585, 628 
Hsematoma, 58 

of pia mater, 294 
Haematometra, 582^ 
Haematophilia, 677 
Hgematoxylin, formula for. 52 
Haematozoon of malaria, 223 
Hasmoglobinsemia, 64 
Haemorrhage, 57 

by diapedesis, 58 



INDEX. 



707 



Ha3morrhage by rhexis, 57 

Haemorrhagic diathesis, 677 
infarction, 61 

Haemorrhoids, 573 

Hanging. 8, 684 

Hardening and preserving tissues, 47 

JIayem's solution for blood examination, 
68 

Head, method of examination of, 9 

Healing, 97, 128 

Heart, abnormal size of, 397 
abscess of, 409 
aneurism of, 411 
atrophy of, 398 

atrophy of pericardial fat of, 403 
calcification of, 403 
changes in position of, 397 
degeneration of, acute, 401 
degeneration of, amyloid, 402 
degeneration of. fatty, 401 
degeneration of, hyalin, 403 
dilatation of, 400 
fatty infiltration of, 403 
fragmentation of myocardium, 404 
hypertrophy of (see Myocarditis), 

404, 409 
intiammation of endocardial lin- 
ing, 404 
inflammation of, syphilitic, 410 
inflammation of, tubercular, 280 
lipomatosis of, 403 
malformations of, 395 
myomalacia of, 404 
parasites of, 412 
preservation of tissues of, 24 
rupture of, 397 
thrombosis of, 411 
tumors of, 412 
valves, aneurisms of, 410 
valves, fenestration of, 410 
valves, haimorrhage in, 411 
valves, suflSciency of, modes of 

determining, 22 
valves, position of, 22 
valves, vegetations on, 407 
walls, thickness of, 21 
weight of, 21 
wounds of, 397 

Hellebore poisoning, lesions of, 695 

Hepatic artery, 492 
veins, 494 

Hepatitis, acute, 500 

chronic interstitial, 503 
purulent, 500 
syphilitic, 506 
tubercular. 507 

Hepatization in pneumonia. 360 

Hermaphroditism, 623 

Herni;i3 of bladder, 422 
of brain, 31(i 
of uterus, 584 
of vagina, 577 

Histioid tumors. 232 

Jlodgkins disease, 434, 675 

Horseshoe kidney, 543 



IIowHliips lucunae in bone, 640 

Hyalin degeneration, 84 

Hydatids (see Echinococcus), 108 

Hydatid moles, 616 

Hydraemia, 63 

Hydrencephalocele, 318 

Hydrocele, 626 

Hydrocephalus. 293, 296, 297, 298, 315 

Hydrochloric acid poisoning, 690 

Hydrocyanic acid poisoning, 696 

Hydromeningocele, 316 

Hydrometra, 582 

Hydromyelia. 330, 331 

Hydromyelocele, 330 

Hydronephrosis, 558 

Hydrophobia, 219 

Hydrops cystidis fellse, 516 

Hydrorrhachis, 330 

Hydro salpinx, 611 

Hydrostatic test for aeration of lungs, 43 

Hydrothorax, 340 

Hymen, malformations of, 574 

Hyperaemia. 57 

Hyperostosis, 653 

Hyperplasia, 71 

Hypertrophy, 71 

Hyphomycetes, 119 

Hypoblast, 232 

Hypophysis cerebri, 299 

Immunity, 128 

Incarceration of intestine, 464 

Indigo- sulphate poisoning, 689 

Infants, post-mortem examination of, 38 

Infarction, haemorrhagic, from emboli, 
58, 61 
white, 62 

Infection by pyogenic bacteria, 149 

Infectious diseases, 148 

Infiltration, fatty, 78 

Inflammation, 87 

abscess in. 92 
acute degeneration in, 87 
croupous, 100 
diphtheritic, 100 
exudative, 88, 91, 94 
fibrinous, 91 
granulation tissue in, 95 
hiemorrhagic. 91 
healing in. 97, 98 
hyperplastic, 101 
interstitial, 101 
mucous, 91 
necrotic, 91 
parenchymatous. 87 
productive. 101 
pseudo-diphtheritic, 101 
purulent, 91 
repair of wounds by. 94 
reparative. 94 
resolution from. 94 
serous. 91 

special forms of, 102 
suppurative, 91. 92. 152 
tubercular, 172 



"08 



INDEX. 



Inflammation, ulcerative, 92 
Inflammatory fever (see Pyaemia), 157 
Influenza, 202 
Infusoria, 105 
Injection, interstitial, 50 
Injuries, post-mortem, 7 
Insolation, 680 

Intestines, appearances in, at autopsies, 
20 

atresia of, 464 

bacteria in, 478 

cadaveric lividities in, 30 

cloacffi of, 463 

concretions in, 477 

diverticula of, 463 

incarceration of, 464 

intussusception of, 465 

large, inflammation of, 468 

lesions of lymph nodes or 
glands of, 467 

malformations of, 463 

parasites of, 477 

preservation of, 31 

removal of, 30 

rupture of, 466 

small, inflammation of (see 
Enteritis), 466 

small, ulcers of, 468 

transposition of, 466 

tumors of, 475 

wounds of, 466 
Intracanalicular fibroma, 239 
Intussusception of intestine, 465 
Itch insect, 116 

Jalap poisoning, lesions of, 695 

Joints, inflammation of (see Arthritis), 656 

loose bodies in, 660 

tumors of, 659 

Karyokinesis, 72 

Karyomitosis, 72 

Kidney, abscess, 556 

Bright's disease of, forms, 544 

calculi of, 561 

changes in position of, 543 

congestion of, acute, 544 

congestion of, chronic, 551 

cystic, 559 

degeneration of, acute, 544 

degeneration of, amyloid, 555 

degeneration of, chronic, 551 

degeneration, parenchymatous, 

544, 551 
degeneration of, waxy, 555 
embolism of, 557 
hydronephrosis, 558 
inflammation of (see Nephritis), 

546 
inflammation, acute dift'use, 549 
inflammation, exudative, 546 
inflammation, suppurative, 555 
malformations of, 543 
method of preservation of, 28 
parasites of, 563 
thrombosis of, 557 



Kidney, tumors of, 561 

Koch's method of bacterial culture, 



134 



Lang's solution, 49 
Lardaceous degeneration, 80 
Laryngitis, 336 
Larynx, cysts of, 339 

inflammation of (see Laryngitis), 

336 
malformations of, 336 
preservation and removal of, 

method, 26 
tumors of, 339 
Lead poisoning, lesions of, 694 
Leiomyoma, 255 
Lepra, 182 
Leprosy, 182 
Leptothrix buccalis, 143 
Leucocytes, 65 
Leucocythaemia, 66, 875 
Leucocytosis, 66 
Leucomaines, 123 
Leukcemia. 66, 651, 675 
pseudo-, 675 
Lightning, death from, 682 
Li pyemia, 69 
Lipoma, 251 

Lipomatosis of heart, 403 
Lips, 441 
Liver, abscess of, 590 

abscess of, amcebic, 501 

abscess, metastatic, 501 

abscess, pysemic, 501 

amyloid, 496 

anaemia of, 490 

artery, hepatic, lesions of, 492 

atrophy of, 494 

atrophy of, acute yellow, 499 

bronze, 498 

changes in position, 489 

cirrhosis of. 503 

cloudy swelling in, 494 

congestion of, 491 

degeneration of, acute. 494 

degeneration of, amyloid. 496 

degeneration of, fatty, 496 

degeneration, parenchymatous, 494 

degeneration of, waxy, 496 

displacements of, 490 

fatty infiltration of, 495 

gummata of. 507 

haemoirhage of, 492 

hypergemia of, 490 

inflammation of (see Hepatitis), 
500 

lymDhatic tissue, hyperplasia of, 
509 

malformations of, 489 

nutmeg, 491 

parasites of, 512 

pigmentation of, 498 

rupture of, 492 

size and weight of, 33 

tumors of. 509 

veins of, 492 



INDEX. 



7f)lj 



Liver, waxy, 496 

wounds of, 492 
Lividity, cadaveric, 4 
Lobelia poisoning, lesions of, 699 
Locomotor ataxia, 327 
Loffler's blue solution, 133 
Louse. 116 

Lungs, atelectasis of, 358 
congestion of, 354 
emphysema of, 356 
gangrene of, 358 
haemorrhage, 355 
infarctions of, 355 
inflammation of (see Pneumonia), 

forms, 359 
inflammation of, syphilitic, 386 
inflammation of, tubercular, 
373 
injuries of, 354 
malformations of, 354 
oedema of, 354 
parasites of, 389 
perforations of, 354 
preservation of, 25 
removal of, 24 
rupture of, 233 
tumors of, 387 
Lupus, 180 

follicles, 431 
Lymph glands (see Lymph nodes), 430 
nodes, 300 

nodes, atrophy of, 438 
nodes, degeneration of, amyloid, 

438 
nodes, degeneration of, hyalin, 

438 
nodes, hyperplasia of, 439 
nodes, inflammation of, 431 
nodes, inflammation of, chronic, 

433 
nodes, inflammation of, syphili- 
tic, 437 
nodes, inflammation of, tubercu- 
lar, 436 
nodes, inflammation, with cheesy 

degeneration of, 435 
nodes, intestinal, lesions of, 192 
nodes, parasites of, 440 
nodes, pigmentation of, 434 
nodes, tumors of, 440 
nodules, 431 
vessels, 428 

vessels, inflammation of, 429 
vessels, inflammation of, syphili- 
tic, 430 
vessels, inflammation of, tubercu- 
lar, 429 
vessels, tumors of, 430 
Lymphangiectasis, 430 
Lymphangioma, 259, 430 
Lymphangitis, 429, 430 
Lymphatic tissue, 430 
Lymphocytes. 65 
Lymphoma, 439 
Lymphosarcoma. 245 



Macrocytes, 64 
Macroglossia, 430 
Malarial fevers, 221 
Malignant oRdema, 204 
pustule, 167 
Mamma, female, cysts of, 619 

female, haemorrliage of, 616 
female, inflammation of (see 

Mastitis), 616 
female, malformations of, 616 
female, tumors of, 619 
male, lesions of, 634 
Mastitis, 616-619 
Measles, 217 
''Measly pork." 107 
Mediastinum, general character of, 380 
inflammations of, 389 
tumors of, 390 
Melansemia, 67 
Melano-carcinoma, 276 

sarcoma, 245 
Meningitis, acute, 286 

acute cerebro-spinal, 155 
chronic, 290 
exudative, 287 
syphilitic, 294 
tubercular, 291 
Merismopedia, 141 
Metaplasia, 74 

Methyl blue stain for bacteria, 130 
violet stain for amyloid, 81 
Metritis, 589 
Microcephalia, 316 
Micrococci, 140 
Micrococcus gonorrhopse, 165 
luteus, 141 
tetragenus, 152 
ureae, 142 
Microcytes, 64 

Microscope for studying bacteria, 133 
Microsporon furfur, 146 
Micro-organisms, 119 
Microtomes, 46 
Miliary tubercles, 173 
Milk as culture medium for bacteria, 

136 
Mitosis, 72 
Moles, hydatid, 616 
Molluscum contagiosum, 104 
Morbus maculosus, 076 
Moulds. 119, 147 

Mouth, inflammation of (see Stomatitis). 
442 
gangrene of, 443 
malformations of. 441 
tumors of. 443 
Mucous degeneration, 82 

polyp, 241 
Midler's fluid, formula and uses, 47 
Mumps, 535 
Muscle, atrophy, simple. 664 

atroi>hy. progressive. 664 
degeneration of fatty. 667 
degeneration of hyalin. 667 
htvmorrhage of, 661 



710 



INDEX. 



Muscle, hypertrophy of, 668 

infarction of, 661 

inflammation of (see Myositis), 
661 

parasites in, 669 

pseudo-hypertrophy of, 667 

rupture of, 661 

tumors of, 669 

wounds of, 661 
Museum specimens, methods of preserva- 
tion, 53 
Mycosis intestinalis, 168, 477 
Myelitis. 323 
Myelocytes, 66, 651 
Myeloid sarcoma, 245 
Myeloplaxes, 501 
Myocarditis, 409 
Myoma, 255 

laevicellulare, 255 

striocellulare, 256 
Myomalacia of heart, 404 
Myositis, interstitial, 661 
Myxoedema, 539 
Myxoma, 239 



Nsevi, vascular, 259 
Neck, cysts of, 446 

fistulaB of, 447 
Necrosis, 76 

coagulation, 76 
of bone, 646 
Kematoda, 111 
Nephritis, 544 

chronic diffuse, with exuda- 
tion, 552 
chronic diffuse, without exu^ 

dation, 553 
chronic pyelo-, 556 
diffuse, acute, 549 
diffuse, chronic, 552, 553 
exudative, acute, 546 
parenchymatous, acute, 545 
parenchymatous, chronic, 551 
peri-, 560 
pyelo , 555 
suppurative, 555 
tubercular, 557 
Nerves, hardening of, 18 

method of preparation of, 333 
peripheral, changes in, after di- 
vision, 331 
peripheral, inflammation of (see 

Neuritis), 332 
peripheral, tumors of, 333 
Nerve tissue, preparation of, 333 
Nervous system, lesions of, 279 
Neuritis, 332 
Neuro-epithelioma, 273 
Neuroma, 256 
Neutrophile leucocytes, 65 
Nitric acid poisoning, lesions of, 689 

acid, decalcifying for, 47 
Nitrobenzole poisoning, lesions of, 696 
Nux vomica poisoning, jesions of, 698 



Obliterating endarteritis, 416 
Odontoma, 253 
(Edema glottidis, 339 
(Esophagitis, 448 
(Esophagus, cysts of, 450 

dilatation, 447, 449 
inflammation of (see CP^so- 

phagitis), 448 
malformations of. 446 
preservation of, 26 
rupture of. 449 
stenosis of, 450 
tumors of, 451 
ulceration of, 449 
Oidium albicans, 147 
Oligocythaemia, 64 
Omentum, 19 
Oophoritis, acute, 601 
chronic, 601 
syphilitic, 604 
tubercular, 603 
Opium poisoning, lesions of, 696 
Orchitis, acute, 628 
chronic, 628 
syphilitic, 631 
tubercular, 629 
Osmic acid as hardening agent, 48, 67 
Osteitis, 638 

condensing, 639, 641 
rarefying, 639 
suppurative, 642 
syphilitic, 643 
tubercular, 642 
Osteoblasts, 637 
Osteoclasts, 640 
Osteoid tissue, 100 
Osteoma, 253 
Osteomalacia, 650 
Osteomyelitis, idiopathic, 645 
traumatic, 645 
Osteophytes, 253, 637 
Osteoporosis, 639 
Osteo-sarcoma, 246 
sclerosis, 641 
Ovarian cyst-adenoma, 604 
Ovaries, cysts of, 610 

haemorrhage, 600 
hyperagmia, 600 
inflammation of. 601 
malformations of, 600 
position, changes in, 600 
size, changes in, 600 
tumors of, 604 
Ovaritis, 601 
Ovula Nabothi, 443 
Oxalic acid poisoning, lesions of, 690 
Oxyuris vermicularis, 112, 477 

Pacchionian bodies, 10 

Pachydermia laryngis, 337 

Pachymeningitis, acute, 280 

Pagefs disease, 104, 617 

Pancreas, atrophy of, 531 
calculi in, 533 
degenerations of, 532 



INDEX. 



711 



Pancreas, displacements of, 533 
fat necrosis of. 532 
gangrene of, 530 
haemorrhage of. 530 
inflammation of (see Pancreati- 
tis), 530, 531 
malformations of, 533 
preservation and removal of, 

33 
tumors of. 533 
Pancreatic ducts, dilatation of, 533 

foreign bodies in, 583 
Pancreatitis, 530 
Papilloma, 238 
Parablastic tissues, 231 
Paraffin, 50 
Parametritis, 589 
Paraphimosis, 624 
Parasites, animal, 103 

animal, methods of studying, 

117 
vegetable, 119 
Parenchymatous degeneration, 77 
Paresis of the insane, 313 
Parotid gland, lesions of, 535 
Parovarium, cysts of, 611 
Pearls, epithelial, 270 
Pediculus capitis, 117 
Penis, calcification of, 625 
enlargement of, 623 
haemorrhage of, 684 
inflammation of, 624 
injury of, 624 
malformations of, 622 
ossification of, 625 
tumors of, 624 
ulcers of, 624 
Pentastomum denticulatum, 477 
Periarteritis, 414 
Pericarditis, 393 
Pericardium, dropsy of, 392 

haemorrhage of, 392 
inflammation of (see Peri- 
carditis), 393 
injuries of, 392 
pneumonatosis of, 392 
tumors of, 394 
Perihepatitis, 508 
Perimetritis, 589 
Periostitis, 636 
Periosteum, 484 
Perisplenitis, 526 
Peritoneum, cysts of, 488 

inflammation of, 478 
malformations of, 478 
parasites of, 488 
tumors of, 486 • 
Peritonitis, acute, 479 

cellular, acute, 479 
cellular, chro-jic, 482 
chronic, with adhesions. 483 
chronic, with serum, librin, 

and pus, 484 
chronic, with thickening of 
the peritoneum, 483 



Peritonitis, exudative, 479 

haemorrhagic, 485 
tubercular, 485 
Pernicious anaemia, 565 
Petechise, 58 
Petri's plates, 136 
Phagocytes, 99, 129 
Pharyngitis, 447 

Pharynx, inflammation of (see Pharyngi- 
tis), 447 
malformations of, 446, 447 
preservation and removal of, 

26 
tumors of, 451 
ulceration of, 448 
Phimosis, 624 
Phlebitis, 426 

syphilitic, 428 
tubercular, 427 
uterine. 590 
Phleboliths, 60, 425 
Phloroglucin for decalcifying, 47 
Phosphorus poisoning, lesions of, 691 
Phthisis, acute catarrhal, 379 
acute pulmonary, 379 
chronic, 383 
Pia mater, anaemia of, 285 

mater, fatty degeneration in, 289 
mater, hyperaemia, haemorrhage of.. 

285 
mater, inflammation of, 286 
mater, oedema of, 285 
mater, parasites in, 295 
mater, pigmentation of, 286 
mater, structure of. 284 
mater, tumors of, 294 
mater spinalis, 317 
mater spinalis, haemorrhage of, 317 
mater spinalis, inflammation of, 318 
mater spinalis, parasites of, 319 
mater spinalis, tumors of, 319 
Picric acid in decalcifying, 47 
Pigmentation, 85 
PinAvorm, 112 
Pineal gland. 299 
Pituitary body, 299 
Pityriasis versicolor, 146 
Placenta, apoplexy of, 615 
cysts of, 615 
degeneration of, 615 
haMuorrhage in. 614 
inflammation of, 615 
Placentitis, 615 
Plasmodium malaria\ 105, 221 
Plate cultures of bacteria. 136 
Pleura, 340 

luvmorrhage of. 340 
inflammation of, 340 
tumors of. 348 
Pleural cavities, examination of. 24 
Pleurisy, acute. 341 

artificial, in dog, 342 
chronic. 347 
tubercular. 347 
with etYusiou, 341 



71- 



INDEX. 



Pleurisy with fibrin, 3-tl 

with fibrin, serum, and pus, 345 
Pleuritis (see Pleurisy), 346 
Pneumococcus of FrO.nkel, 152, 156, 162, 
163, 362 
of Friedldnder , 204 
Pneumonia, acute lobar, 359 

acute lobar, with new con- 
nective tissue, 362 
broncho-, 364 
catarrhal, 364 
complicating, 369 
forms of, 359 
interstitial, 372 
lobar, 359 
lobular, 364 
of heart disease, 370 
secondary, 369 
syphilitic, 386 
tubercular, 373 
Pneumotoxin, 163 
Poikilocytes, 64 

Poisoning, lesions of, by aconite, 699 
lesions of, by alcohol. 697 
lesions of, by aloes, 695 
lesions of, by ammonia, 691 
lesions of, by arsenic, 692 
lesions of, by belladonna, 699 
lesions of, by cantharides, 696 
lesions of, by carbolic acid, 

697 
lesions of, by carbonic acid, 

699 
lesions of, by carbonic oxide, 

699 
lesions of, by chloral hydrate, 

698 
lesions of, by chloroform, 69S- 
lesions of, by colchicum, 695 
lesions of, by colocynth, 695 
lesions of, by conium, 699 
lesions of, by copper, 695 
lesions of, bv corrosive subli- 
mate, 694' 
lesions of, by croton oil, 695' 
lesions of, by cyanide of po- 
tassium, 696 
lesions of, by digitalis, 699 
lesions of, by elaterium, 695 
lesions of, by ether. 698 
lesions of, by fungi, 696 
lesions of, by gamboge, 695 
lesions of, by hellebore, 695 
lesions of, by hydrochloric 

acid, 690 
lesions of, by hydrocyanic 

acid, 696 
lesions of, by jalap, 695 
lesions of, by lead, 694 
lesions of, by lobelia, 699 
lesions of, by nitric acid, 689 
lesions of, by nitrobenzole, 696 
lesions of, bv nux vomica, 

698 
lesions of, by opium, 696 



Poisoning, lesions of, by oxalic acid, 690 
lesions of, by phosphorus, 691 
lesions of, by potash, 691 
lesions of, by potassium ni- 
trate, 691 
lesions of, by potassium 

cyanide, 696 
lesions of, by savin, 695 
lesions of, by scammony, 695 
lesions of, by soda, 691 
lesions of, by stramonium, 699 
lesions of, by strychnine, 698 
lesions of, by sulphuric acid, 

688 
lesions of, by tartar emetic, 

695 
lesions of, by tartaric acid, 690 
lesions of, by turpentine, 695 
lesions of, by vegetable irri- 
tants, 695 
lesions of, by veratria, 695 
removal of intestines and 
stomach in cases of, 37 
Poliomyelitis, 324 
Polyp, mucous, 241 
Porencephalia, 308 
Portal vein, lesions of, 492 
Post-mortem changes in abdominal or- 
gans, 19 
cooling of the body, 6 
decomposition, 5 
discoloration, 5 
examination in suspected 

poisoning, 37 
examination, exteroal in- 
spection in, 4 
examination, internal ex- 
amination in, 9 
examination, observations 

on identity in, 4 
examination, reasons for 

making, 3 
fractures, 8 
injuries, 8 

putrefactive changes, 4, o 
rigidity or rigor mortis, 6 
wounds. 8 
Potash poisoning, lesions of, 691 
Potassium cj^anide poisoning, lesions of, 
696 
nitrate poisoning, lesions of, 
691 
Potato as culture medium for bacteria, 

135 
Predisposition to infectious disease, 127 
Pregnancy, extra-uterine, 613 
Preservation of specimens, methods, 48, 

54 
Proglottides of tapeworm, 106 
Prostate, atrophy of, 638 
calculi in, 634 
cysts, 634 

hypertrophy of, 632 
inflammation of, 633 
parasites in, 634 



INDEX. 



713 



Prostate, tumors of, 633 
Proteus vulgaris, 143 
Protozoa, 103 

methods of study, 105 
Psammoma, 249, 288 
Pseudo-diphtheritic bacillus, 200 

hermaphroditism, 623 

leuksemia, 439, QIC 
Psorospermiae, 104 
Ptomaines, 123 
Puerperal fever, 158 
Purpura haemorrhagica, 676 
Pus cells, 93 

Putrefaction, bacteria in, 122 
Pyaemia, 157 
Pyelo-nephritis, 555, 556 
Pyogenic bacteria, 149, 370 
Pyo-salpinx, 612 
septicaemia. 157 
pneumothorax, 345 

Rachitis, 647 
Ranula, 445 
Ray fungus, 207 
Rectum, lesions of, 474 
Regeneration, 71, 73 
Relapsing fever, 213 
Respiratory system, 336 
Rhabdomyoma, 256 
Rhabdonema strongyloides, 116 
Rhexis, haemorrhage by, 57 
Rhinoscleroma, 186 
Rickets. 647 
Rigor mortis, 6 

SacclAromyces, 145 

Safranin for staining fresh tissues, 46 

Salivary glands, 535 

Salpingitis, 612 

Saprophytic bacteria, 140 

Sarcina, 141, 142 

Sarcoma, 241 

adeno-, 249 

alveolar, 248 

angio-, 247 

cysto-, 249 

endothelial, 249 

fibro-, 243 

giant celled, 245 

glio-, 245 

lympho-, 245 

melano-, 245 

myeloid, 245 

myxo-, 248 

osteo-, 246 

round-celled, 244 

spindle-celled, 243 
Sarcoptes hominis, 116 
Savin poisoning, lesions of, 695 
Scammony poisoning, lesions of, 695 
Scarlatina, 216 
Scarlet fever, 216 
Scars, disappearance of, in .^kin, 8 
Schistomycetes, 119 
Scirrhous carcinoma, 273 



Sclerosis, multiple, of cord, 326 

posterior spinal, 327 
Scolex of tapeworm, 106 
Scolices of echinococcus, 109 
Scorbutus. 676 
Scrofula, 436 
Scrotum, lesions of, 625 
Scurvy, 675 
Section cutting, 50, 52 
Seminal vesicles, 632 
Septicaemia, 157 
Septic intoxication. 126 
Septico- pyaemia. 157 
Sequestrum, 646 
Serum in inflammation, 88, 90 
Small-pox, 215 

Soda poisoning, lesions of, 691 
Spermatocele, 627 
Spider cells, 254 
Spina bifida, 330 
Spinal cord, 317 

cord, cysts of, 328 

cord, degeneration of, gray, 320 

cord, examination of, 17 

cord, gummata of, 328 

cord, haemorrhage of. 310 

cord, inflammation of, 323 

cord, inflammation of, syphilitic, 

328 
cord, inflammation of, tubercular, 

328 
cord, injuries of, 319 
cord, malformations of. 330 
cord, membranes of, 317 
cord, posterior sclerosis in, 327 
cord, preservation of, 18 
cord, sclerosis of, 326 
cord, syringomyelia, 329 
cord, tumors of, 3'2S 
Spiral-shaped bacteria, 144 
Spirilla, 144 

Spirillum cholerae Asiaticae, 210 . • 
fever, 213 
rubrum, 144 
rugula, 144 
serpens, 141 
tyrogenes, 142 
Spiro-bacteria, 144 
Spirochaete denticola, 144 

Obermeieri, 214 
plicatilis, 144 
Spleen, abscess, 523 

anannia of. 520 
atrophy of, 527 
bacteria in, 529 
congestion of, 521 
degenerations of, 527 
displacements of, 529 
luvmorrhage of. 520 
hypera^mia of, 520 
infarctions of. 521 
inflammation of (see Splenitis), 

leukamiic. 526 

mal format i(Mis of. 529 



714 



INDEX. 



Spleen, parasites of, 528 

pigmentation of, o2S 
rupture of, 519 
sago, 527 
tumors of, 528 
wounds of, 519 
Splenic fever, 167 
tumor. 523 
Splenitis, acute hyperplastic, 522 
chronic indurative, 523 
suppurative. 523 
syphilitic, 525 
tubercular, 525 
Spores of bacteria. 120. 121 
Staiaing methods for tissues, 53 
Staphylococci. 141 

Staphylococcus cereus albus flavus, 152 
epidermidis albus, 151 
gilvus, 152 
pyogenes albus, 151 
pvosrenes aureus, 149, 

'15^7, 106, 200 
pyogenes citreus, 152 
salivarius pyogenes, 152 
Stomacace. 442 

Stomach, degenerations of, 463 
dilatation of. 460 
erosions of. hiemorrhagic, 459 
examination of. 20, 31 
haemorrhage. 454 
inflammation of (see Gastritis), 

454 
injuries of. 454 
malformations of, 458 
post-mortem changes in, 453 
tumors of, 460 
ulcers of. 457. 460 
Stomatite, ulcero-membraneuse, 442 
Stomatitis, 444 

ulcerosa, 442 
Stramonium poisoning, lesions of, 699 
Strangulation, 8, 684 
Streptococci, 141 

in uterine phlebitis, 590 
Streptococcus erysipelatis, 153 

pvo2:enes, 149, 151, 156, 
"'160, 200 
Strongylus gigas, 112 

longevaginatus, 112 
Struma, 537 

Strychnia poisoning, lesions of. 698 
Sublimate, corrosive. in fixing blood cells, 

68 
Sublingual gland, 535 
Submaxillary gland, 535 
Suffocation. 683 
Suggillations, 58 
Sufphuric acid poisoning, lesions of, 

688 
Sunstroke, 680 

Suprarenal capsules, lesions of, 541 
Syphilis, 184 

congenital, bones in, 643 
Svphilitic inflammation, 184 
Syringomyelia, 329 



Tabes, 327 

Tienia cucumerina. 110 
echinococcus. 108 
flavo-punctata, 110 
madagascariensis. 110 
mediocanellata, 108, 478 
nana, 110 
sasinata, 108 
solium. 106, 478 
Tapeworm, 106 

Tartar emetic poisoning, lesions of. 695 
Tattoo marks, disappearance of, 8 
Temperature, post mortem elevation of. 

5, 6 
Teratoma myxomatodes, 390 
Testicle, atrophv of. 6:^6 

cysts of. 632 

inflammation of (see Orchitis), 
628 

malformations of, 626 

parasites of, 632 

tumors of, 631 
Tetanus, 201 

Thorax, examination of organs of, 18 
Thrombosis, 59 
Thrombus, 59 
Thymus, 540 

Thyroid gland, lesions of, 537 
Tongue, hypertrophy of. 444 

inflammation of. 445 

malformations of. 444 
Tonsils, 447 

Toxalbumins, 123, 125. 157 
Toxin. 127, 157 
Trachea, inflammation of. 336 

malformations of, 336 w 

tumors of, 340 
Tracheitis, 336 
Transudation, 57, 59 
Traumatic fever, 157 
Trematoda, 106 
Trichina spiralis, 113, 477 
Trichomonas vaginalis, 105 
Trichophyton tonsurans,. 146 
Tricocephalus dispar, 113, 477 
Tubercle bacilli, 170 

bacilli, dead, action of. 176 

bacilli, staining of, 177 

granula, 174 

tissue, 173 
Tubercles, structure and form of, 173 
Tubercular inflammation, 172, 174 
Tuberculosis, 170 

acute miliary, 374 
chronic, of lungs, 377, 383 
subacute miliary. 377 
Tumors, bacteria and other organisms 
in, 229, 230 

cause of, 228 

characters of, general, 224 

classification of, 231 

complex nomenclature of, 235 

epithelial, 261 

growth, mode of 225 

malignancv of, 227 



INDEX. 



715 



Tumors, metastasis of, 226 

mixed forms of, 233 

preservation of, 235 

special forms of, 237 

teratoid, 233 
Turpentine poisoning, lesions of, 695 
Typhoid fever, bacillus of, 195 

fever, lesions of, 189 
Typhus fever, 218 

recurrens, 213 

Urethra, inflammation of (see Urethritis), 
572 
malformations of, 570 
perforations of, 571 
prolapse of, 571 
rupture of, 571 
strictures of, 571 
tumors of, 573 
V70unds of. 571 
Urethritis, catarrhal, 572 
croupous. 573 
tubercular, 573 
Urinary apparatus, 543 
Uterine mucous membrane, hyperplasia 

of, 588 
Uterus, cysts of, 599 

degenerations of, 591 
haematocele of, 585 
haemorrhage of, 584 «» 

herniae of, 584 
liypersemia of. 584 
inflammation of (see Metritis and 

Endometritis), 585, 589 
inversion of, 583 
malformations of, 580 
malpositions of, 582 
parasites of, 599 
perforation of, 584 
rupture of, 584 
tumors of, 591 
ulceration of, 591 

Vagina, cysts of, 580 

dilatation of, 577 
fistula} of, 578 
gangrene of, 579 
hernioe of, 577 

inflammation of (see Vaginitis), 
578, 579 



Vagina, lengthening of, 577 

malformations of, 577 
narrov^ing of, 577 
parasites of, 580 
prolapse of, 577 
tumors of, 579 
wounds of, 57^ 
Vaginitis, 578, 579 
Vascular system. 392 
Vein stones, 60, 425 
Veins, dilatation of, 425 

inflammation of (see Phlebitis), 

426 
parasites in, 428 
phleboliths, 60, 425 
rupture of, 426 
tumors of, 428 
wounds of, 426 
Veratria poisoning, lesions of, 695 
Vermiform appendix, 474 
Vulva, cysts of. 576 

haemorrhage of, 574 
hyperaemia of, 574 
inflammation of, 575 
lupus of, 576 
malformations of, 574 
noma of, 575 
oedema of, 575 
tumors of, 576 

Wax for embedding, 50 

Waxy degeneration, 80 

Weigerfs haematoxyliu method for stain- 
ing nerve tissue, 334 
modification of Grams meth- 
od. 132 

Whip worm, 78 

Worms, 106 

Wounds, healing of, 94 
post-mortem, 8 

Xanthin calculi, 570 

Yeasts, 119, 145, 147 
Yellow fever, 5i20 

ZiehVs solution for staining bacteria, 177 
Zooglcea colonies of bacteria, 120 



